Glycosuria, Renal
Sodium-Glucose Transporter 2
Fanconi Syndrome
Diabetes Mellitus
Kidney
Diabetes Mellitus, Experimental
Hexoses
Glucose Tolerance Test
Glycosuria
Glucosides
Glucose
Hepatocyte Nuclear Factor 1-alpha
Insulin
Hepatocyte Nuclear Factor 1
Kidney Tubules
Hepatocyte Nuclear Factor 1-beta
Diabetes Mellitus, Type 2
Diabetes Mellitus, Type 1
Effectiveness of a prevention program for diabetic ketoacidosis in children. An 8-year study in schools and private practices. (1/293)
OBJECTIVE: To shorten the period of carbohydrate intolerance preceding the diagnosis of IDDM in children. RESEARCH DESIGN AND METHODS: The incidence of diabetic ketoacidosis (DKA) was studied in newly diagnosed diabetic children aged 6-14 years, in the area of Parma, Italy, 8 years after an information program on DKA was introduced to teachers, students, parents, and pediatricians. Information was provided by displaying a poster with a few practical messages in 177 primary and secondary public schools. The pediatricians working in the same area were given equipment for the measurement of both glycosuria and blood glucose levels, as well as cards listing guidelines for the early diagnosis of diabetes, to be given to patients. A toll-free number was also provided. Clinical and laboratory features of 24 young diabetic patients diagnosed in the Parma area (group 1) were compared with those of 30 patients coming from two nearby areas in which no campaign for the prevention of DKA had been carried out (group 2). RESULTS: From 1 January 1991 to 31 December 1997, DKA was diagnosed in 3 children from group 1 (12.5%) and in 25 children from group 2 (83.0%) (chi 2 = 26.8; P = 0.0001). The three cases of DKA in group 1 were observed in 1991 (n = 1) and in 1992 (n = 2). No patients from the Parma area who had DKA were admitted to our unit after 1992. The duration of symptoms before diagnosis was 5.0 +/- 6.0 and 28.0 +/- 10.0 days (P < 0.0001), in groups 1 and 2, respectively, Metabolic derangements were less severe in patients of group 1 than in those of group 2. Hospitalization for the treatment of overt diabetes and for the teaching of self-management of the disease lasted 5.4 +/- 1.2 days in group 1 and 13.3 +/- 2.4 days in group 2 (P = 0.002). The total cost of the 8-year campaign was $23,470. CONCLUSIONS: The prevention program for DKA in diabetic children aged 6-14 years, carried out in the Parma area during the last 8 years, was successful. Thanks to this program, cumulative frequency of DKA in new-onset IDDM decreased from 78% during 1987-1991 to 12.5% during 1991-1997. None of the newly diagnosed diabetic children aged 6-14 years and from the Parma area were ever admitted to the hospital for DKA after 1992. (+info)Effect of glucose and pH on uropathogenic and non-uropathogenic Escherichia coli: studies with urine from diabetic and non-diabetic individuals. (2/293)
It is generally assumed that one of the reasons why diabetics are more susceptible to urinary tract infections than non-diabetics is their 'sweet urine'. However, very little information is available on this subject. Therefore, the growth rates of different Escherichia coli strains were studied in human urine with and without added glucose and with and without a constant pH, and compared with their growth rates in Mueller-Hinton broth (MHB). Eight isolates were used (three from blood cultures from urosepsis patients, two urinary isolates, two faecal isolates and one laboratory strain K12). All isolates grew better in MHB than in urine, but with the exception of the laboratory strain, they had the same growth rate in urine. No significant difference was found between the growth rate in urine from diabetics without glucosuria and that in urine from non-diabetics. The addition of glucose (up to a concentration of 1000 mg/dl) to urine and MHB enhanced the growth rate of all isolates. However, very high concentrations of glucose (up to 10000 mg/dl) in urine and MHB caused a decrease in bacterial growth rate when the urinary pH was not kept constant. The stationary phase was reached later and the final bacterial yield was greater when the urine was made less acidic. As the uropathogenic strains did not grow better in urine than the other isolates, it may be concluded that better growth in urine is not one of the causes of the greater virulence of these strains. (+info)Relations between exposure to arsenic, skin lesions, and glucosuria. (3/293)
OBJECTIVES: Exposure to arsenic causes keratosis, hyperpigmentation, and hypopigmentation and seemingly also diabetes mellitus, at least in subjects with skin lesions. Here we evaluate the relations of arsenical skin lesions and glucosuria as a proxy for diabetes mellitus. METHODS: Through existing measurements of arsenic in drinking water in Bangladesh, wells with and without arsenic contamination were identified. Based on a questionnaire, 1595 subjects > or = 30 years of age were interviewed; 1481 had a history of drinking water contaminated with arsenic whereas 114 had not. Time weighted mean arsenic concentrations and mg-years/l of exposure to arsenic were estimated based on the history of consumption of well water and current arsenic concentrations. Urine samples from the study subjects were tested by means of a glucometric strip. People with positive tests were considered to be cases of glucosuria. RESULTS: A total of 430 (29%) of the exposed people were found to have skin lesions. Corresponding to drinking water with < 0.5, 0.5-1.0, and > 1.0 mg/l of arsenic, and with the 114 unexposed subjects as the reference, the prevalence ratios for glucosuria, as adjusted for age and sex, were 0.8, 1.4, and 1.4 for those without skin lesions, and 1.1, 2.2, and 2.6 for those with skin lesions. Taking exposure as < 1.0, 1.0-5.0, > 5.0-10.0 and > 10.0 mg-years/l of exposure to arsenic the prevalence ratios, similarly adjusted, were 0.4, 0.9, 1.2, and 1.7 for those without and 0.8, 1.7, 2.1, and 2.9 for those with skin lesions. All series of risk estimates were significant for trend, (p < 0.01). CONCLUSIONS: The results suggest that skin lesions and diabetes mellitus, as here indicated by glucosuria, are largely independent effects of exposure to arsenic although glucosuria had some tendency to be associated with skin lesions. Importantly, however, glucosuria (diabetes mellitus) may occur independently of skin lesions. (+info)Vasopressin contributes to hyperfiltration, albuminuria, and renal hypertrophy in diabetes mellitus: study in vasopressin-deficient Brattleboro rats. (4/293)
Diabetic nephropathy represents a major complication of diabetes mellitus (DM), and the origin of this complication is poorly understood. Vasopressin (VP), which is elevated in type I and type II DM, has been shown to increase glomerular filtration rate in normal rats and to contribute to progression of chronic renal failure in 5/6 nephrectomized rats. The present study was thus designed to evaluate whether VP contributes to the renal disorders of DM. Renal function was compared in Brattleboro rats with diabetes insipidus (DI) lacking VP and in normal Long-Evans (LE) rats, with or without streptozotocin-induced DM. Blood and urine were collected after 2 and 4 weeks of DM, and creatinine clearance, urinary glucose and albumin excretion, and kidney weight were measured. Plasma glucose increased 3-fold in DM rats of both strains, but glucose excretion was approximately 40% lower in DI-DM than in LE-DM, suggesting less intense metabolic disorders. Creatinine clearance increased significantly in LE-DM (P < 0.01) but failed to increase in DI-DM. Urinary albumin excretion more than doubled in LE-DM but rose by only 34% in DI-DM rats (P < 0.05). Kidney hypertrophy was also less intense in DI-DM than in LE-DM (P < 0.001). These results suggest that VP plays a critical role in diabetic hyperfiltration and albuminuria induced by DM. This hormone thus seems to be an additional risk factor for diabetic nephropathy and, thus, a potential target for prevention and/or therapeutic intervention. (+info)Is there a role for glycosuria testing in sub-Saharan Africa? (5/293)
BACKGROUND: With increasing urbanization and westernization, rates of diabetes in sub-Saharan Africa (sSA) are likely to rise. Early detection and intervention plays an important role in delaying development of complications. In sSA in particular there is need for an affordable, reliable, safe, feasible test to avert human suffering and exhausting already stressed health facilities. METHODS: Data from two large community-based studies were used to assess the value of glycosuria testing in the detection of diabetes in adults in a sub-Saharan country. A first study (A) tested participants for glycosuria by dipstick; if positive, fasting capillary glucose was measured. A later study (B) measured glucose concentration in venous blood 2 h after a 75-g glucose load; if glycaemia was > or = 10 mmol/l, urine was tested for glycosuria. RESULTS: The positive predictive value of glycosuria for a diagnosis of diabetes (fasting glucose > or = 6.7 mmol/l) was 48%. Sensitivity was 64% (57% if a 2-h-value > or = 10 mmol/l was used as gold standard). Sensitivity was higher among overweight and/or hypertensive subjects, among elderly people in the urban area, and among subjects with higher blood glucose levels. Extrapolated specificity was 99.7%, and the likelihood ratio 190. CONCLUSIONS: Glycosuria testing can identify a considerable number of undiagnosed diabetic patients when specially targeted at high-risk groups (obese, hypertensive, or elderly people). Dipstick glycosuria testing is an appropriate, safe, feasible test for sSA, where the prevalence of diabetes is expected to increase considerably in the near future. (+info)A new mouse model of spontaneous diabetes derived from ddY strain. (6/293)
By the selective breeding of obese male mice of the ddY strain and using indices of the heavy body weight and appearance of urinary glucose, we established two inbred strains in 1992: one with obesity and urinary glucose (Tsumura, Suzuki, Obese Diabetes: TSOD) and the other without them (Tsumura, Suzuki, Non Obesity: TSNO). The male TSOD mice constantly showed signs of obesity and urinary glucose with increases in food and water intake, body weight and some fat weight. The body mass index (BMI) clearly showed moderate obesity. Increases in the levels of diabetic blood parameters (glucose, insulin and lipids) were also found in males, in which the levels of blood glucose and insulin were high to the ages past the growth peak. In the histological studies, pancreatic islets of the TSOD males were found hypertrophic without any signs of insulitis or fibrous formation. Among these diabetic characteristics, some of which were similar to the reported models of non-insulin-dependent diabetes mellitus (NIDDM), the stable appearances of the hyperglycemia, the hyperinsulinemia and the hypertrophy of pancreatic islets to the ages past the growth peak were the prominent features. In these respect the TSOD mouse may be a useful model for researching the mechanisms of human diabetes and its complications. (+info)Targeted disruption of CDK4 delays cell cycle entry with enhanced p27(Kip1) activity. (7/293)
The mechanism by which cyclin-dependent kinase 4 (CDK4) regulates cell cycle progression is not entirely clear. Cyclin D/CDK4 appears to initiate phosphorylation of retinoblastoma protein (Rb) leading to inactivation of the S-phase-inhibitory action of Rb. However, cyclin D/CDK4 has been postulated to act in a noncatalytic manner to regulate the cyclin E/CDK2-inhibitory activity of p27(Kip1) by sequestration. In this study we investigated the roles of CDK4 in cell cycle regulation by targeted disruption of the mouse CDK4 gene. CDK4(-/-) mice survived embryogenesis and showed growth retardation and reproductive dysfunction associated with hypoplastic seminiferous tubules in the testis and perturbed corpus luteum formation in the ovary. These phenotypes appear to be opposite to those of p27-deficient mice such as gigantism and gonadal hyperplasia. A majority of CDK4(-/-) mice developed diabetes mellitus by 6 weeks, associated with degeneration of pancreatic islets. Fibroblasts from CDK4(-/-) mouse embryos proliferated similarly to wild-type embryonic fibroblasts under conditions that promote continuous growth. However, quiescent CDK4(-/-) fibroblasts exhibited a substantial ( approximately 6-h) delay in S-phase entry after serum stimulation. This cell cycle perturbation by CDK4 disruption was associated with increased binding of p27 to cyclin E/CDK2 and diminished activation of CDK2 accompanied by impaired Rb phosphorylation. Importantly, fibroblasts from CDK4(-/-) p27(-/-) embryos displayed partially restored kinetics of the G(0)-S transition, indicating the significance of the sequestration of p27 by CDK4. These results suggest that at least part of CDK4's participation in the rate-limiting mechanism for the G(0)-S transition consists of controlling p27 activity. (+info)Vasopressin and urinary concentrating activity in diabetes mellitus. (8/293)
In diabetes mellitus (DM), the high urine flow rate suggests that urinary concentrating capacity is impaired. However, several studies have shown that vasopressin is elevated in DM and the consequences of this elevation have not yet been characterized. This study reevaluated renal function and water handling in male Wistar rats with Streptozotocin-induced DM, and in control rats. During five weeks after induction of DM, urine was collected in metabolic cages and a blood sample was drawn during the third week. Control rats (CONT) were studied in parallel. On week 3, urine flow rate was tenfold higher in DM than in CONT rats and urinary osmolality was reduced by half along with a markedly higher osmolar excretion (DM/CONT = 5.87), due for a large part to glucose but also to urea (DM/CONT = 2.49). Glucose represented 52% of total osmoles (90.3 +/- 6.5 mmol/d out of 172 +/- 14 mosm/d). Free water reabsorption was markedly higher in DM rats compared to CONT (326 +/- 24 vs 81 +/- 5 ml/d). In other rats treated in the same way, urinary excretion of vasopressin was found to be markedly elevated (15.1 +/- 4.1 vs 1.44 +/- 0.23 ng/d). In DM rats, glucose concentration in urine was 17 fold higher than in plasma, and urea concentration 14 fold higher. Both urine flow rate and free water reabsorption were positively correlated with the sum of glucose and urea excretions (r = 0.967 and 0.653, respectively) thus demonstrating that the urinary concentrating activity of the kidney increased in proportion to the increased load of these two organic solutes. These results suggest that vasopressin elevation in DM contributes to increase urinary concentrating activity and thus to limit water requirements induced by the metabolic derangements of DM. The possible deleterious consequences of sustained high level of vasopressin in DM are discussed. (+info)Renal glycosuria is a medical condition characterized by the presence of glucose in the urine due to defective renal tubular reabsorption, despite normal blood glucose levels. In healthy individuals, the kidneys are able to reabsorb all filtered glucose back into the bloodstream. However, in renal glycosuria, the kidneys fail to reabsorb some or all of the glucose, leading to its excretion in the urine.
Renal glycosuria can be congenital or acquired. Congenital renal glycosuria is a rare inherited disorder caused by mutations in the SLC5A2 gene, which encodes the glucose transporter 2 (GLUT2) protein responsible for glucose reabsorption in the kidneys. Acquired renal glycosuria can occur as a result of damage to the renal tubules due to various causes such as diabetes, hypertension, or certain medications.
Renal glycosuria is usually asymptomatic and discovered incidentally during routine urinalysis. However, in some cases, it may lead to increased urinary frequency, urgency, and polyuria due to the osmotic diuretic effect of glucose in the urine. If left untreated, renal glycosuria can increase the risk of urinary tract infections and kidney stones. Treatment is typically not necessary for asymptomatic individuals with renal glycosuria, but monitoring blood glucose levels is recommended to rule out underlying diabetes mellitus.
Sodium-Glucose Transporter 2 (SGLT2) is a medically recognized term referring to a specific protein that plays a crucial role in the reabsorption of glucose in the kidneys. It is a type of membrane transport protein located in the proximal convoluted tubule of the nephron, where it actively transports glucose and sodium ions from the urine back into the bloodstream.
In healthy individuals, SGLT2 is responsible for reabsorbing about 90% of the filtered glucose, maintaining normal blood glucose levels. However, in certain medical conditions like diabetes, the amount of glucose in the blood can be significantly higher than normal. As a result, SGLT2 inhibitors have been developed as a class of medications to block this transporter's function, thereby increasing glucose excretion through urine and lowering blood glucose levels.
SGLT2 inhibitors are often prescribed in combination with other diabetes medications to help manage type 2 diabetes more effectively. Common SGLT2 inhibitors include canagliflozin, dapagliflozin, and empagliflozin.
Fanconi syndrome is a medical condition that affects the proximal tubules of the kidneys. These tubules are responsible for reabsorbing various substances, such as glucose, amino acids, and electrolytes, back into the bloodstream after they have been filtered through the kidneys.
In Fanconi syndrome, there is a defect in the reabsorption process, causing these substances to be lost in the urine instead. This can lead to a variety of symptoms, including:
* Polyuria (excessive urination)
* Polydipsia (excessive thirst)
* Dehydration
* Metabolic acidosis (an imbalance of acid and base in the body)
* Hypokalemia (low potassium levels)
* Hypophosphatemia (low phosphate levels)
* Vitamin D deficiency
* Rickets (softening and weakening of bones in children) or osteomalacia (softening of bones in adults)
Fanconi syndrome can be caused by a variety of underlying conditions, including genetic disorders, kidney diseases, drug toxicity, and heavy metal poisoning. Treatment typically involves addressing the underlying cause, as well as managing symptoms such as electrolyte imbalances and acid-base disturbances.
Keratosis, in general, refers to a skin condition characterized by the abnormal growth or development of keratin, a protein that forms part of the outer layer of the skin (epidermis). There are several types of keratosis, including:
1. Seborrheic Keratosis: benign, often pigmented, rough, and scaly growths that can appear anywhere on the body. They tend to increase in number with age.
2. Actinic Keratosis: rough, scaly patches or spots on the skin that are caused by long-term exposure to sunlight or artificial UV light. These have the potential to develop into squamous cell carcinoma, a type of skin cancer.
3. Solar Keratosis: another term for actinic keratosis, as it is primarily caused by sun damage.
4. Keratosis Pilaris: a common condition where small, rough bumps appear on the skin, often on the arms, thighs, or cheeks. These are caused by excess keratin blocking hair follicles.
5. Follicular Keratosis: a disorder characterized by the formation of horny plugs within the hair follicles, leading to rough, sandpaper-like bumps on the skin.
6. Intraepidermal Keratosis: a term used to describe the abnormal accumulation of keratin in the epidermis, which can lead to various skin conditions.
It's important to consult with a healthcare professional or dermatologist for proper diagnosis and treatment if you suspect having any form of keratosis.
Diabetes Mellitus is a chronic metabolic disorder characterized by elevated levels of glucose in the blood (hyperglycemia) due to absolute or relative deficiency in insulin secretion and/or insulin action. There are two main types: Type 1 diabetes, which results from the autoimmune destruction of pancreatic beta cells leading to insulin deficiency, and Type 2 diabetes, which is associated with insulin resistance and relative insulin deficiency.
Type 1 diabetes typically presents in childhood or young adulthood, while Type 2 diabetes tends to occur later in life, often in association with obesity and physical inactivity. Both types of diabetes can lead to long-term complications such as damage to the eyes, kidneys, nerves, and cardiovascular system if left untreated or not well controlled.
The diagnosis of diabetes is usually made based on fasting plasma glucose levels, oral glucose tolerance tests, or hemoglobin A1c (HbA1c) levels. Treatment typically involves lifestyle modifications such as diet and exercise, along with medications to lower blood glucose levels and manage associated conditions.
Blood glucose, also known as blood sugar, is the concentration of glucose in the blood. Glucose is a simple sugar that serves as the main source of energy for the body's cells. It is carried to each cell through the bloodstream and is absorbed into the cells with the help of insulin, a hormone produced by the pancreas.
The normal range for blood glucose levels in humans is typically between 70 and 130 milligrams per deciliter (mg/dL) when fasting, and less than 180 mg/dL after meals. Levels that are consistently higher than this may indicate diabetes or other metabolic disorders.
Blood glucose levels can be measured through a variety of methods, including fingerstick blood tests, continuous glucose monitoring systems, and laboratory tests. Regular monitoring of blood glucose levels is important for people with diabetes to help manage their condition and prevent complications.
Hyperglycemia is a medical term that refers to an abnormally high level of glucose (sugar) in the blood. Fasting hyperglycemia is defined as a fasting blood glucose level greater than or equal to 126 mg/dL (milligrams per deciliter) on two separate occasions. Alternatively, a random blood glucose level greater than or equal to 200 mg/dL in combination with symptoms of hyperglycemia (such as increased thirst, frequent urination, blurred vision, and fatigue) can also indicate hyperglycemia.
Hyperglycemia is often associated with diabetes mellitus, a chronic metabolic disorder characterized by high blood glucose levels due to insulin resistance or insufficient insulin production. However, hyperglycemia can also occur in other conditions such as stress, surgery, infection, certain medications, and hormonal imbalances.
Prolonged or untreated hyperglycemia can lead to serious complications such as diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state (HHS), and long-term damage to various organs such as the eyes, kidneys, nerves, and blood vessels. Therefore, it is essential to monitor blood glucose levels regularly and maintain them within normal ranges through proper diet, exercise, medication, and lifestyle modifications.
Hematuria is a medical term that refers to the presence of blood in urine. It can be visible to the naked eye, which is called gross hematuria, or detected only under a microscope, known as microscopic hematuria. The blood in urine may come from any site along the urinary tract, including the kidneys, ureters, bladder, or urethra. Hematuria can be a symptom of various medical conditions, such as urinary tract infections, kidney stones, kidney disease, or cancer of the urinary tract. It is essential to consult a healthcare professional if you notice blood in your urine to determine the underlying cause and receive appropriate treatment.
A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:
1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.
2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.
3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).
4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.
5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.
Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.
I couldn't find a medical definition specifically for "Diabetes Mellitus, Experimental." However, I can provide you with information about experimental diabetes research and its relevance to understanding the disease.
Experimental diabetes models are used in biomedical research to study the pathophysiology of diabetes mellitus and to test potential therapies or treatments. These models can be broadly categorized into two types: chemically-induced and genetically modified.
1. Chemically-induced diabetes models: These involve administering chemicals, such as alloxan or streptozotocin, to animals (commonly mice or rats) to destroy their pancreatic β-cells, which produce insulin. This results in hyperglycemia and symptoms similar to those seen in type 1 diabetes in humans.
2. Genetically modified diabetes models: These involve altering the genes of animals (commonly mice) to create a diabetes phenotype. Examples include non-obese diabetic (NOD) mice, which develop an autoimmune form of diabetes similar to human type 1 diabetes, and various strains of obese mice with insulin resistance, such as ob/ob or db/db mice, which model aspects of type 2 diabetes.
These experimental models help researchers better understand the mechanisms behind diabetes development and progression, identify new therapeutic targets, and test potential treatments before moving on to human clinical trials. However, it's essential to recognize that these models may not fully replicate all aspects of human diabetes, so findings from animal studies should be interpreted with caution.
Hexoses are simple sugars (monosaccharides) that contain six carbon atoms. The most common hexoses include glucose, fructose, and galactose. These sugars play important roles in various biological processes, such as serving as energy sources or forming complex carbohydrates like starch and cellulose. Hexoses are essential for the structure and function of living organisms, including humans.
A Glucose Tolerance Test (GTT) is a medical test used to diagnose prediabetes, type 2 diabetes, and gestational diabetes. It measures how well your body is able to process glucose, which is a type of sugar.
During the test, you will be asked to fast (not eat or drink anything except water) for at least eight hours before the test. Then, a healthcare professional will take a blood sample to measure your fasting blood sugar level. After that, you will be given a sugary drink containing a specific amount of glucose. Your blood sugar levels will be measured again after two hours and sometimes also after one hour.
The results of the test will indicate how well your body is able to process the glucose and whether you have normal, impaired, or diabetic glucose tolerance. If your blood sugar levels are higher than normal but not high enough to be diagnosed with diabetes, you may have prediabetes, which means that you are at increased risk of developing type 2 diabetes in the future.
It is important to note that a Glucose Tolerance Test should be performed under the supervision of a healthcare professional, as high blood sugar levels can be dangerous if not properly managed.
Glycosuria is a medical term that refers to the presence of glucose in the urine. Under normal circumstances, the kidneys are able to reabsorb all of the filtered glucose back into the bloodstream. However, when the blood glucose levels become excessively high, such as in uncontrolled diabetes mellitus, the kidneys may not be able to reabsorb all of the glucose, and some of it will spill over into the urine.
Glycosuria can also occur in other conditions that affect glucose metabolism or renal function, such as impaired kidney function, certain medications, pregnancy, and rare genetic disorders. It is important to note that glycosuria alone does not necessarily indicate diabetes, but it may be a sign of an underlying medical condition that requires further evaluation by a healthcare professional.
Proteinuria is a medical term that refers to the presence of excess proteins, particularly albumin, in the urine. Under normal circumstances, only small amounts of proteins should be found in the urine because the majority of proteins are too large to pass through the glomeruli, which are the filtering units of the kidneys.
However, when the glomeruli become damaged or diseased, they may allow larger molecules such as proteins to leak into the urine. Persistent proteinuria is often a sign of kidney disease and can indicate damage to the glomeruli. It is usually detected through a routine urinalysis and may be confirmed with further testing.
The severity of proteinuria can vary, and it can be a symptom of various underlying conditions such as diabetes, hypertension, glomerulonephritis, and other kidney diseases. Treatment for proteinuria depends on the underlying cause and may include medications to control blood pressure, manage diabetes, or reduce protein loss in the urine.
Glucosides are chemical compounds that consist of a glycosidic bond between a sugar molecule (typically glucose) and another non-sugar molecule, which can be an alcohol, phenol, or steroid. They occur naturally in various plants and some microorganisms.
Glucosides are not medical terms per se, but they do have significance in pharmacology and toxicology because some of them may release the sugar portion upon hydrolysis, yielding aglycone, which can have physiological effects when ingested or absorbed into the body. Some glucosides are used as medications or dietary supplements due to their therapeutic properties, while others can be toxic if consumed in large quantities.
Glucose is a simple monosaccharide (or single sugar) that serves as the primary source of energy for living organisms. It's a fundamental molecule in biology, often referred to as "dextrose" or "grape sugar." Glucose has the molecular formula C6H12O6 and is vital to the functioning of cells, especially those in the brain and nervous system.
In the body, glucose is derived from the digestion of carbohydrates in food, and it's transported around the body via the bloodstream to cells where it can be used for energy. Cells convert glucose into a usable form through a process called cellular respiration, which involves a series of metabolic reactions that generate adenosine triphosphate (ATP)—the main currency of energy in cells.
Glucose is also stored in the liver and muscles as glycogen, a polysaccharide (multiple sugar) that can be broken down back into glucose when needed for energy between meals or during physical activity. Maintaining appropriate blood glucose levels is crucial for overall health, and imbalances can lead to conditions such as diabetes mellitus.
Hepatocyte Nuclear Factor 1-alpha (HNF1A) is a transcription factor that plays a crucial role in the development and function of the liver. It belongs to the family of winged helix transcription factors and is primarily expressed in the hepatocytes, which are the major cell type in the liver.
HNF1A regulates the expression of various genes involved in glucose and lipid metabolism, bile acid synthesis, and drug metabolism. Mutations in the HNF1A gene have been associated with maturity-onset diabetes of the young (MODY), a form of diabetes that is typically inherited in an autosomal dominant manner and often diagnosed in early adulthood. These mutations can lead to impaired insulin secretion and decreased glucose tolerance, resulting in the development of diabetes.
In addition to its role in diabetes, HNF1A has also been implicated in liver diseases such as nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD). Dysregulation of HNF1A has been shown to contribute to the development and progression of these conditions by altering the expression of genes involved in lipid metabolism, inflammation, and fibrosis.
Insulin is a hormone produced by the beta cells of the pancreatic islets, primarily in response to elevated levels of glucose in the circulating blood. It plays a crucial role in regulating blood glucose levels and facilitating the uptake and utilization of glucose by peripheral tissues, such as muscle and adipose tissue, for energy production and storage. Insulin also inhibits glucose production in the liver and promotes the storage of excess glucose as glycogen or triglycerides.
Deficiency in insulin secretion or action leads to impaired glucose regulation and can result in conditions such as diabetes mellitus, characterized by chronic hyperglycemia and associated complications. Exogenous insulin is used as a replacement therapy in individuals with diabetes to help manage their blood glucose levels and prevent long-term complications.
Hepatocyte Nuclear Factor 1 (HNF-1) is a transcription factor that plays a crucial role in the development and function of the liver. It is composed of two subunits, HNF-1α and HNF-1β, which heterodimerize to form the functional transcription factor.
HNF-1 is involved in the regulation of genes that are essential for glucose and lipid metabolism, bile acid synthesis, and transport processes in the liver. Mutations in the genes encoding HNF-1α or HNF-1β can lead to various monogenic forms of diabetes, such as MODY (Maturity Onset Diabetes of the Young), and other liver diseases.
HNF-1α is primarily expressed in the liver, kidney, and pancreas, while HNF-1β is expressed in a wider range of tissues, including the liver, kidney, pancreas, intestine, and genitourinary tract. Both subunits recognize and bind to specific DNA sequences, known as HNF-1 binding sites, to regulate the transcription of their target genes.
Kidney tubules are the structural and functional units of the kidney responsible for reabsorption, secretion, and excretion of various substances. They are part of the nephron, which is the basic unit of the kidney's filtration and reabsorption process.
There are three main types of kidney tubules:
1. Proximal tubule: This is the initial segment of the kidney tubule that receives the filtrate from the glomerulus. It is responsible for reabsorbing approximately 65% of the filtrate, including water, glucose, amino acids, and electrolytes.
2. Loop of Henle: This U-shaped segment of the tubule consists of a thin descending limb, a thin ascending limb, and a thick ascending limb. The loop of Henle helps to concentrate urine by creating an osmotic gradient that allows water to be reabsorbed in the collecting ducts.
3. Distal tubule: This is the final segment of the kidney tubule before it empties into the collecting duct. It is responsible for fine-tuning the concentration of electrolytes and pH balance in the urine by selectively reabsorbing or secreting substances such as sodium, potassium, chloride, and hydrogen ions.
Overall, kidney tubules play a critical role in maintaining fluid and electrolyte balance, regulating acid-base balance, and removing waste products from the body.
Hepatocyte Nuclear Factor 1-beta (HNF-1β) is a transcription factor that plays crucial roles in the development and function of various organs, including the liver, kidneys, pancreas, and genitourinary system. It belongs to the PPAR/RXR heterodimer family of transcription factors and regulates the expression of several genes involved in cell growth, differentiation, metabolism, and transport processes.
In the liver, HNF-1β is essential for maintaining the structural organization and function of hepatocytes, which are the primary functional cells of the liver. It helps regulate the expression of genes involved in glucose and lipid metabolism, bile acid synthesis, and detoxification processes.
Mutations in the HNF-1β gene have been associated with several genetic disorders, such as maturity-onset diabetes of the young (MODY5), renal cysts and diabetes syndrome (RCAD), and congenital abnormalities of the kidneys and urinary tract (CAKUT). These conditions often present with a combination of liver, pancreas, and kidney dysfunctions.
Diabetes Mellitus, Type 2 is a metabolic disorder characterized by high blood glucose (or sugar) levels resulting from the body's inability to produce sufficient amounts of insulin or effectively use the insulin it produces. This form of diabetes usually develops gradually over several years and is often associated with older age, obesity, physical inactivity, family history of diabetes, and certain ethnicities.
In Type 2 diabetes, the body's cells become resistant to insulin, meaning they don't respond properly to the hormone. As a result, the pancreas produces more insulin to help glucose enter the cells. Over time, the pancreas can't keep up with the increased demand, leading to high blood glucose levels and diabetes.
Type 2 diabetes is managed through lifestyle modifications such as weight loss, regular exercise, and a healthy diet. Medications, including insulin therapy, may also be necessary to control blood glucose levels and prevent long-term complications associated with the disease, such as heart disease, nerve damage, kidney damage, and vision loss.
Diabetes Mellitus, Type 1 is a chronic autoimmune disease characterized by the destruction of insulin-producing beta cells in the pancreas, leading to an absolute deficiency of insulin. This results in an inability to regulate blood glucose levels, causing hyperglycemia (high blood sugar). Type 1 diabetes typically presents in childhood or early adulthood, although it can develop at any age. It is usually managed with regular insulin injections or the use of an insulin pump, along with monitoring of blood glucose levels and adjustments to diet and physical activity. Uncontrolled type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, blindness, and cardiovascular disease.
Kidney disease, also known as nephropathy or renal disease, refers to any functional or structural damage to the kidneys that impairs their ability to filter blood, regulate electrolytes, produce hormones, and maintain fluid balance. This damage can result from a wide range of causes, including diabetes, hypertension, glomerulonephritis, polycystic kidney disease, lupus, infections, drugs, toxins, and congenital or inherited disorders.
Depending on the severity and progression of the kidney damage, kidney diseases can be classified into two main categories: acute kidney injury (AKI) and chronic kidney disease (CKD). AKI is a sudden and often reversible loss of kidney function that occurs over hours to days, while CKD is a progressive and irreversible decline in kidney function that develops over months or years.
Symptoms of kidney diseases may include edema, proteinuria, hematuria, hypertension, electrolyte imbalances, metabolic acidosis, anemia, and decreased urine output. Treatment options depend on the underlying cause and severity of the disease and may include medications, dietary modifications, dialysis, or kidney transplantation.
Glycosuria
Renal glycosuria
Neonatal hypoglycemia
Renal threshold
Glossary of diabetes
George Graham (physician)
Goulstonian Lecture
Arnaldo Cantani
Stanley Rossiter Benedict
Charles Richard Box
Nicolae Paulescu
Ketonuria
Abderhalden-Kaufmann-Lignac syndrome
Urinalysis
Frederick Madison Allen
History of diabetes
Oxyhyperglycemia
NOD mice
Robertson Fotheringham Ogilvie
Relative density
Vilhjalmur Stefansson
Tolbutamide
Nicolae Blatt
Diet in diabetes
Desonide
Entecavir
Philip Hugh-Jones
Fanconi syndrome
Renal glucose reabsorption
Splay (physiology)
Glycosuria - Wikipedia
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Alimentary glycosuria
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HYPERGLYCEMIA10
- It can be due to HYPERGLYCEMIA or genetic defects in renal reabsorption (RENAL GLYCOSURIA). (uams.edu)
- The most easily recognized symptoms of type 1 diabetes mellitus (T1DM) are secondary to hyperglycemia, glycosuria, and DKA. (medscape.com)
- The main symptoms of hyperglycemia are secondary to osmotic diuresis and glycosuria. (medscape.com)
- It is a result of hyperglycemia (high blood sugar levels ), where the kidney filters malfunction and lead to glycosuria. (canadianinsulin.com)
- Clinical signs reflect hyperglycemia with resultant glycosuria. (merckvetmanual.com)
- Diagnosis is made by documenting persistent hyperglycemia and glycosuria. (merckvetmanual.com)
- Hyperglycemia, glycosuria, hyperuricemia. (druglib.com)
- Hyperglycemia results in glycosuria and an osmotic diuresis. (vin.com)
- These conditions may include Cushing's syndrome, hyperglycemia, and glycosuria. (canadapharmacy.com)
- We have been taught that in hyperglycemia, when you have high blood sugar, you spill a lot of sugar and then you have glycosuria. (medscape.com)
Renal8
- Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys (such as Fanconi syndrome), producing a condition termed renal glycosuria. (wikipedia.org)
- Additionally, SGLT2 inhibitor medications ("gliflozins" or "flozins") produce glycosuria as their primary mechanism of action, by inhibiting sodium/glucose cotransporter 2 in the kidneys and thereby interfering with renal glucose reabsorption. (wikipedia.org)
- If the RTG is so low that even normal blood glucose levels produce the condition, it is referred to as renal glycosuria. (wikipedia.org)
- The suspected causes of renal glycosuria can be that the level of blood glucose could get too high due to which the renal tubules cannot reabsorb it completely or, there might be failure of the tubules to reabsorb all the glucose. (diabetesinformationhub.com)
- Hyperglycemic rats showed diabetic complications including polydipsia, polyuria, glycosuria, renal hypertrophy and increased glomerular filtration rate. (nih.gov)
- 3. Primary renal glycosuria (Fanconi syndrome): A proximal tubular defect results in renal glycosuria leading to an osmotic diuresis. (vin.com)
- Threshold for renal glycosuria is a blood glucose of 180-220 mg/dl (dog) and 240-300 mg/dl (cat). (vin.com)
- it is called renal glycosuria, it does not require any treatment. (ndtv.com)
Urine8
- Glycosuria is the excretion of glucose into the urine. (wikipedia.org)
- Glycosuria leads to excessive water loss into the urine with resultant dehydration, a process called osmotic diuresis. (wikipedia.org)
- Alimentary glycosuria is a temporary condition, when a high amount of carbohydrate is taken, it is rapidly absorbed in some cases where a part of the stomach is surgically removed, the excessive glucose appears in urine producing glycosuria. (wikipedia.org)
- However, when glycosuria occurs, the kidneys are unable to take enough glucose out from the urine before it releases from the body. (canadianinsulin.com)
- While having a small amount of glucose in the urine is considered normal, glycosuria is indicated when a urine sample shows 0.25 mg/ml or more of glucose. (canadianinsulin.com)
- Third, a laboratory technician will test and determine if the presence of sugar in your urine suggests glycosuria. (canadianinsulin.com)
- Glycosuria is the presence of reducing substances (glucose, galactose, lactose, and fructose) in the urine. (labpedia.net)
- Glycosuria (glucose in your urine) may indicate poor glucose control. (roadtrucker.com)
Proteinuria and glycosuria1
- Initial laboratory data include a urinalysis showing 3+ proteinuria and glycosuria. (cdc.gov)
Produce glycosuria1
- These drugs produce glycosuria. (medscape.com)
Diabetes9
- Glycosuria is nearly always caused by elevated blood glucose levels, most commonly due to untreated diabetes mellitus. (wikipedia.org)
- Definition noun A form of glycosuria caused by the incapacity of the liver and other tissues to metabolize glucose faster than the rate of intestinal absorption of glucose Supplement Synonym(s): alimentary diabetes digestive glycosuria See also: alimentary canal glycosuria diabetes. (biologyonline.com)
- Glycosuria is a condition interlinked with diabetes. (canadianinsulin.com)
- Like other diabetes-related diseases, symptoms of glycosuria do not necessarily appear, thus, making people asymptomatic. (canadianinsulin.com)
- Diabetes is the leading cause of glycosuria. (canadianinsulin.com)
- Since the condition is linked with blood sugar malfunction, diabetes has been deemed the culprit as to why glycosuria continues to exist in many people with varying blood glucose levels. (canadianinsulin.com)
- However, your attending doctor will most likely advise you to take preventive measures like proper diabetes management to inhibit glycosuria from happening in the future. (canadianinsulin.com)
- If diabetes causes glycosuria, proper blood sugar management is necessary to treat the existing condition. (canadianinsulin.com)
- Non-diabetic glycosuria and non-glycosuric diabetes. (nih.gov)
Polyuria2
Urinalysis1
- Urinalysis revealed glycosuria and ketonuria. (bmj.com)
Primary1
- Even glycosuria testing can be helpful at a primary care level. (bvsalud.org)
Symptoms1
- What are the symptoms of glycosuria? (canadianinsulin.com)
Glucose reabsorption1
- it is classical glycosuria, with decline in both, glucose threshold and maximal glucose reabsorption rate. (diabetesinformationhub.com)
MeSH1
- Glycosuria" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (uams.edu)
Topic1
- This graph shows the total number of publications written about "Glycosuria" by people in UAMS Profiles by year, and whether "Glycosuria" was a major or minor topic of these publications. (uams.edu)
Concept1
- As a clinician, I have always been a little wary of this whole concept of worsening glycosuria. (medscape.com)
Tests1
- Glycosuria tests performed by diabetics at home. (cdc.gov)
Conditions1
- These three conditions represent different stages of glycosuria. (who.int)
Hyperglycemia6
- The most easily recognized symptoms of type 1 diabetes mellitus (T1DM) are secondary to hyperglycemia, glycosuria, and DKA. (medscape.com)
- The main symptoms of hyperglycemia are secondary to osmotic diuresis and glycosuria. (medscape.com)
- It can be due to HYPERGLYCEMIA or genetic defects in renal reabsorption (RENAL GLYCOSURIA). (ouhsc.edu)
- Clinical signs reflect hyperglycemia with resultant glycosuria. (merckvetmanual.com)
- Abnormal glucose tolerance and insulin response were seen when pancreatic IRI was depleted by about one-third, while fasting hyperglycemia and gross glycosuria occurred when the depletion had reached two-thirds and three-quarters, respectively. (jci.org)
- Systemic absorption of topical steroids has produced reversible hypothalamic pituitary-adrenal (HPA) axis suppression, manifestations of Cushing's syndrome, hyperglycemia, and glycosuria in some patients. (prescriptiondrugs.com)
Proteinuria2
Serum glucose3
- During long-time follow up, the two patients had frequent unproportional renal glycosuria in the morning even when their fasting serum glucose was only slightly increased. (nih.gov)
- Urine examination showed mild albuminuria and glycosuria (serum glucose was normal) with no pus cells. (rcpe.ac.uk)
- The relationship between the dose of intravenously administered streptozotocin (a N-nitroso derivative of glucosamine) and the diabetogenic response has been explored by use of the following indices of diabetogenic action: serum glucose, urine volume, and glycosuria, ketonuria, serum immunoreactive insulin (IRI), and pancreatic IRI content. (jci.org)
Osmotic diuresis1
- Glycosuria leads to excessive water loss into the urine with resultant dehydration, a process called osmotic diuresis. (wikipedia.org)
Renal glucosuria1
- Renal glycosuria, also known as renal glucosuria, is a rare condition in which the simple sugar glucose is eliminated (excreted) in the urine despite normal or low blood glucose levels. (diabeteshealthmatters.com)
Glucose into the urine1
- Glycosuria is the excretion of glucose into the urine. (wikipedia.org)
Excretion3
- Non-diabetic Glycosuria , also known as Renal Glycosuria, is a rare inherited condition involving the excretion of glucose in the urine in detectable amounts, even though the blood sugar level is in a normal range. (diabeteshealthmatters.com)
- Option B. Excretion of more sugar in urine is defined as glycosuria. (safalta.com)
- Glucose excretion increases as a result of increased glomerular filtration rate of glucose Glycosuria is therefore quite common in pregnancy and is not usually related to a high blood glucose level. (slideshare.net)
Symptoms2
- What are the symptoms for nondiabetic glycosuria? (diabeteshealthmatters.com)
- Oral administration of amellin relieves symptoms of glycosuria, reduces hyperglycaemia and increases RBC count. (pfaf.org)
SGLT21
- Additionally, SGLT2 inhibitor medications ("gliflozins" or "flozins") produce glycosuria as their primary mechanism of action, by inhibiting sodium/glucose cotransporter 2 in the kidneys and thereby interfering with renal glucose reabsorption. (wikipedia.org)
Urine glucose1
- Renal glycosuria can cause urine glucose levels to be high even if blood glucose levels are normal. (healthline.com)
Reabsorption2
- Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys (such as Fanconi syndrome), producing a condition termed renal glycosuria. (wikipedia.org)
- 1 Proximal renal tubular acidosis is characterised by defective proximal tubular reabsorption associated with phosphaturia, glycosuria, aminoaciduria, bicarbonaturia resulting in hypophosphataemia, hypokalaemia and metabolic acidosis. (rcpe.ac.uk)
Excessive1
- Alimentary glycosuria is a temporary condition, when a high amount of carbohydrate is taken, it is rapidly absorbed in some cases where a part of the stomach is surgically removed, the excessive glucose appears in urine producing glycosuria. (wikipedia.org)
Urinary1
- • Glycosuria can be a cause, of urinary tract infection. (slideshare.net)
Medications1
- Is there a cure/medications for nondiabetic glycosuria? (diabeteshealthmatters.com)
Condition2
- If the RTG is so low that even normal blood glucose levels produce the condition, it is referred to as renal glycosuria. (wikipedia.org)
- When renal glycosuria occurs as an isolated finding with otherwise normal kidney function, the condition is thought to be inherited as an autosomal recessive trait. (diabeteshealthmatters.com)
Treatment1
- Not everyone with glycosuria is unwell or needs treatment. (diabeteshealthmatters.com)
Year1
- This graph shows the total number of publications written about "Glycosuria" by people in this website by year, and whether "Glycosuria" was a major or minor topic of these publications. (ouhsc.edu)