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Renal Threshold For Glucose Is Decreased In

Renal Threshold - An Overview | Sciencedirect Topics

Renal Threshold - An Overview | Sciencedirect Topics

The renal threshold for glucose in the dog is about 11.1mmol/l (200mg/dl) so that the detection of even trace amounts of glucose in the urine is an important finding and warrants further consideration. In virtually all cases of diabetes suspected on the basis of persistent glycosuria alone, the diagnosis can be later confirmed. Renal diabetes (i.e., low renal threshold for glucose) is an extremely rare occurrence and, if it does occur, can be detected by finding a normal blood glucose in the presence of the glucosuria. Transient glucosurias may occur for 1 to 1h after a heavy carbohydrate meal, but a 2-h postprandial glucosuria is a strong indication of diabetes. Currently, detection of glucosuria using the urinalysis sticks is the most common method of point-of-care evaluation of the clinical success of insulin therapy. There are disadvantages to this system because of owner difficulties, inconsistencies, and inaccuracies. The FrAm method, whereby only biweekly blood samplings need be taken, can have decided advantages in following the course of insulin therapy. An elevated urinary specific gravity (SG) has in the past been considered to be a good indicator of glucosuria and, hence, of diabetes. SG is a measure of the concentration of solutes in the urine, principally the cations (Na+, K+, ), and urea. The observed SG of urine is the result of the additive effect of the contributions of all these solutes. It is for this reason that the osmolality of any fluid, urine or plasma, can be estimated by simply adding up the major anions and cations expressed in mmols/l (see the chapter on acid-base). Albumin in urine increases the SG by 0.003 units for each 10g/l (1g/dl), whereas glucose increases it by 0.004 units for each 55mmol/l (1g/dl). Even though the presence of gluco Continue reading >>

Renal Glucose Threshold - General Practice Notebook

Renal Glucose Threshold - General Practice Notebook

Glucose is the main source of energy in eukaryotes and the main fuel providing energy for regular metabolic activity in humans as a polar molecule, glucose is not soluble in the plasma membrane and must be transported across it by carrier proteins, named glucose transporters glucose transporters are divided into two families: the facilitative diffusion glucose transporters (GLUTs) both GLUTs and SGLTs belong to one of the 43 families of solute carrier genes (SLC1-SLC43) glucose transporters play an essential role in the maintenance of euglycemia, not only by determining glucose uptake in all cellular types, but also by releasing glucose from the liver when circulating glucose levels decrease also these transporters are responsible for absorbing glucose from the diet in the intestine, and for reabsorbing the glucose from the glomerular filtrate in kidneys transepithelial glucose transport in cells from the small intestine, the renal proximal tubules and salivary gland ducts occurs by the coordinate action of SGLTs allowing glucose influx through the luminal membrane, and GLUTs allowing glucose efflux through the basolateral membrane Filtration and the reabsorption of glucose in the kidney for a healthy adult, approximately 180g of glucose is filtered by the glomerulus every day under normal circumstances, almost all of this glucose is reabsorbed with less than 1% being excreted in the urine glucose reabsorption in the tubules is a multi-step process involving several transport mechanisms glucose is filtered through the tubule and then transported via the tubular epithelial cells through the basolateral membrane into the peritubular capillary. Under optimal conditions, when tubular glucose load is approximately 120mg/min or less, there is no glucose loss in urine however Continue reading >>

Glycosuria

Glycosuria

Glycosuria or glucosuria is the excretion of glucose into the urine. Ordinarily, urine contains no glucose because the kidneys are able to reabsorb all of the filtered glucose from the tubular fluid back into the bloodstream. Glycosuria is nearly always caused by elevated blood glucose levels, most commonly due to untreated diabetes mellitus. Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys (such as Fanconi syndrome), producing a condition termed renal glycosuria.[1] Glycosuria leads to excessive water loss into the urine with resultant dehydration, a process called osmotic diuresis. 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 glucosuria. Pathophysiology[edit] Blood is filtered by millions of nephrons, the functional units that comprise the kidneys. In each nephron, blood flows from the arteriole into the glomerulus, a tuft of leaky capillaries. The Bowman's capsule surrounds each glomerulus, and collects the filtrate that the glomerulus forms. The filtrate contains waste products (e.g. urea), electrolytes (e.g. sodium, potassium, chloride), amino acids, and glucose. The filtrate passes into the renal tubules of the kidney. In the first part of the renal tubule, the proximal tubule, glucose is reabsorbed from the filtrate, across the tubular epithelium and into the bloodstream. The proximal tubule can only reabsorb a limited amount of glucose. When the blood glucose level exceeds about 160 – 180 mg/dl, the proximal tubule becomes overwhelmed and begins to excrete glucose in the urine. Approximate correlation between dipstick designation and Continue reading >>

Glycosuria

Glycosuria

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. Glycosuria is the term for glucose present in urine, in amounts that can be detected by the usual techniques. Pathogenesis Virtually all the glucose that is filtered through the glomeruli is reabsorbed by the proximal renal tubule and so glycosuria represents an abnormal state. The amount of glucose not reabsorbed by the kidneys is usually less than 0.1%. Adults excrete about 65 mg of glucose per day and standard techniques do not detect this level. There are two basic causes of glycosuria. One is that the level of blood glucose is so high that the renal tubules are unable to reabsorb all that is presented. The other is a failure of the tubules to reabsorb all glucose at a level where this should be possible. The latter is called renal glycosuria. The level of blood glucose at which it spills into the urine is called the renal threshold. Under normal circumstances this is around 10 mmol/L. Diastix®, Medi-Test® and Mission Glucose® are plastic strips carrying glucose oxidase and a colour indicator, usually o-toluidine. They are specific and unlikely to give positive results for substances other than glucose. Glucose oxidase strips have superseded older reagents for reducing substances. Elevated blood glucose If glycosuria occurs because a normal renal threshold has been exceeded, this is usually indicative of impaired glucose tolerance or frank diabetes. It can occur in a person who doesn't have diabetes if a substantial amount of food high in sugar is Continue reading >>

Renal Threshold | Canine Diabetes Wiki | Fandom Powered By Wikia

Renal Threshold | Canine Diabetes Wiki | Fandom Powered By Wikia

Renal threshold: When blood glucose rises over a certain level, it spills into the urine. Renal corpuscle. Glomerulus capillaries are #10-the tubules are B and C. In diabetic contexts, the renal threshold refers to the blood glucose level at which the kidneys begin to extract glucose from the blood and excrete it into the urine , causing glycosuria , or glucose in the urine. Polyuria in diabetes shows that the body is unable to metabolize carbohydrates properly. Carbohydrates are turned into glucose, which is sent into the blood to feed the cells. The cells, lacking insulin , can't accept the glucose, so it remains in the blood causing hyperglycemia . The extra glucose in the blood accumulates there until the kidneys see it as an impurity to be filtered out and discarded. This point is known as the renal threshold. When the renal threshold is exceeded, and the excess glucose begins to spill into the urinary tract, the glucose makes the urine attract water in what's known as the osmotic effect . This extra water in the urine causes the excessive urination, dehydrating the body, which in turn causes the excessive drinking of polydipsia . Renal threshold values differ by species. While dogs and humans share the same renal threshold value of 180 mg/dl (10 mmol/L), the renal threshold of cats is 288 mg/dl (16 mmol/L); in cattle it's 108 mg/dl (6 mmol/L). [1] Glucose is filtered through the glomeruli [2] in the kidney; for non-diabetics, all of the glucose is re-absorbed by the renal (kidney) tubules. This means there would be nothing present for a glucose urine test to detect. With hyperglycemia , the kidney tubules are unable to handle and process the amount of glucose they're being presented with, so the glucose winds up in the urine and can be detected in urine glucose t Continue reading >>

Renal Glucosuria

Renal Glucosuria

Background Renal glucosuria is the excretion of glucose in the urine in detectable amounts at normal blood glucose concentrations in the absence of any signs of generalized proximal renal tubular dysfunction due to a reduction in the renal tubular reabsorption of glucose. The revised criteria for diagnosis of this condition includes: a normal oral glucose tolerance test in regard to plasma glucose concentration, normal plasma levels of insulin, free fatty acids, glycosylated hemoglobin, and relatively stable urinary glucose levels (10 to 100 g/d; except during pregnancy, when it may increase) with glucose present in all urine samples. The urine should contain glucose as the only source of carbohydrate, and individuals should have normal carbohydrate storage and use. The inherited form of this disorder is called familial renal glucosuria (FRG) (PRG; OMIM #233100). FRG is a rare disorder due mainly to mutations in the sodium-glucose cotransporter 2 gene (SGLT2) that are responsible for the majority of cases. [1, 2, 3, 4] To date over seventy mutations have been identified including missense mutations, nonsense mutations, small deletions and splicing mutations. Most however are missense mutations. It is usually inherited in a co-dominant fashion with incomplete penetrance. Although the pattern of inheritance that best fits FRG is one of co-dominance, increased glucose excretion was not observed in all individuals with similar or identical mutations. Heterozygosity for mutations suggest a role of nongenetic factors or other genes involved in renal glucose transport. [5] The SGLT2 gene is localized to p11.2 on chromosome 16. It consists of 14 separate exons spanning approximately 7.7kb of genomic DNA, and encodes the 672 amino acid protein SGLT2. Glucosuria in these patients Continue reading >>

Characteristics And Impact Factors Of Renal Threshold For Glucose Excretion In Patients With Type 2 Diabetes Mellitus

Characteristics And Impact Factors Of Renal Threshold For Glucose Excretion In Patients With Type 2 Diabetes Mellitus

Characteristics and Impact Factors of Renal Threshold for Glucose Excretion in Patients with Type 2 Diabetes Mellitus Xiao-Dan Yue ,* Jing-Yu Wang ,* Xin-Rong Zhang , Ju-Hong Yang , Chun-Yan Shan , Miao-Yan Zheng , Hui-Zhu Ren , Yi Zhang , Shao-Hua Yang , Zhen-Hong Guo , Bai Chang , and Bao-Cheng Chang Key Laboratory of Hormones and Development, Ministry of Health, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital, and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China. Key Laboratory of Hormones and Development, Ministry of Health, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital, and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China. Key Laboratory of Hormones and Development, Ministry of Health, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital, and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China. Key Laboratory of Hormones and Development, Ministry of Health, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital, and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China. Key Laboratory of Hormones and Development, Ministry of Health, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital, and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China. Key Laboratory of Hormones and Development, Ministry of Health, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital, and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China. Key Laboratory of Hormones and Development, Ministry of Health, Tianjin Key Laboratory of Metabolic Diseases, Continue reading >>

Jfp - Diabetes Volume 65, No. 12

Jfp - Diabetes Volume 65, No. 12

Role of the Kidney in Type 2 Diabetes and Mechanism of Action of Sodium Glucose Cotransporter-2 Inhibitors The kidneys contribute to overall glucose homeostasis by reabsorbing glucose that is filtered by the kidneys and by producing glucose via gluconeogenesis. Sodium glucose cotransporter-2 (SGLT-2) is responsible for the majority of glucose reabsorption by the kidney. Glucose reabsorption by the kidneys is paradoxically increased in patients with type 2 diabetes owing to increased expression and/or activity of SGLT-2. SGLT-2 inhibitors reduce hyperglycemia by increasing renal glucose excretion and are associated with modest weight loss, decreases in blood pressure, and decreased serum uric acid. The kidney has an important role in glucose homeostasis. It produces glucose via gluconeogenesis, it filters glucose from the blood, and reabsorbs the filtered glucose in the proximal tubule, mainly via the sodium-glucose cotransporter-2 (SGLT-2). SGLT-2 is paradoxically upregulated in individuals with type 2 diabetes (T2D), which results in increased glucose reabsorption and hyperglycemia. This core defect in the pathophysiology of T2D provides the rationale for the use of SGLT-2 inhibitors to increase urinary glucose excretion and reduce hyperglycemia in an insulin-independent manner. Benefits of SGLT-2 inhibitor use in patients with T2D, in addition to improved glycemic control, include modest weight loss, decreased systolic blood pressure, reduced serum uric acid, and reduced risk of cardiovascular events. Common adverse events are urinary tract infection and genital mycotic infections. The risk of hypoglycemia is low with SGLT-2 inhibitors, particularly when they are given as monotherapy. Type 2 diabetes (T2D) is a complex, chronic disease resulting from the interaction Continue reading >>

Glucose

Glucose

Glucose is derived from digestion of dietary carbohydrates, breakdown of glycogen in the liver (glycogenolysis) and production of glucose from amino acid precursors in the liver (gluconeogenesis). In ruminants, the main source of glucose is gluconeogenesis from volatile fatty acids (propionate) absorbed from rumen by bacterial fermentation. Glucose is the principal source of energy for mammalian cells. Uptake is mediated by a group of membrane transport proteins, called glucose transporters (GLU), some of which are insulin-dependent, e.g. GLU-4. Physiology Blood glucose concentration is influenced by hormones which facilitate its entry into or removal from the circulation. The hormones affect glucose concentrations by modifying glucose uptake by cells (for energy production), promoting or inhibiting gluconeogenesis, or affecting glycogenesis (glycogen production) and glycogenolysis and are listed below. The most important hormone involved in glucose metabolism is insulin, which enables energy use and storage and decreases blood glucose concentration. Several hormones oppose the action of insulin and, therefore, will increase blood glucose. The main hormones that mediate this effect are glucagon, growth hormone, catecholamines, and corticosteroids. The increase in blood glucose can occur through inhibition of insulin release, stimulation of glucose-yielding pathways (glycogenolysis, gluconeogenesis), or decrease of glucose uptake or use by tissues. Table 1 below summarizes these effects. Collectively, increases in these insulin opposing hormones can induce a state of insulin resistance. Insulin resistance can also be mediated by inflammatory cytokines (tumor necrosis factor-α [TNF-α]), obesity and pregnancy. Inflammatory cytokines are thought to be responsible for insu Continue reading >>

Renal Glycosuria

Renal Glycosuria

Causes Renal glycosuria is considered an inherited defect of membrane transport (i.e., an abnormal renal transport syndrome). Membrane transport disorders are characterized by abnormalities in the movement (i.e., transport) of one or more compounds across cell membranes. They are thought to result from genetic changes (mutations) causing alterations in specific membrane proteins. As noted above, due to impaired renal tubular functioning, renal glycosuria is characterized by a reduction in the blood glucose concentration at which glucose begins to be excreted in urine (reduced renal threshold for glucose) and, in some instances, a reduction in the maximum rate at which glucose may be reabsorbed into the bloodstream (reduced transport maximum [tubular maximum for glucose or “TmG”]). Researchers have classified renal glycosuria into two major subtypes based upon the presence of such defects: type A (low threshold, reduced TmG) and type B (low threshold, normal TmG). In addition, investigators have described a form of renal glycosuria termed type 0, in which there is complete absence of renal tubular glucose reabsorption. Isolated renal glycosuria with otherwise normal kidney function is thought to be transmitted as an “incompletely” recessive trait (see below). Human traits, including the classic genetic diseases, are the product of the interaction of two genes for that condition, one received from the father and one from the mother. In autosomal recessive disorders, the condition may not appear unless a person inherits a defective (mutated) gene for the same trait from each parent. If an individual receives one normal gene and one gene for the disease, the person will be a carrier for the disease but usually will not show symptoms. The risk of transmitting the dis Continue reading >>

Blood Glucose: Regulation And Renal Threshold

Blood Glucose: Regulation And Renal Threshold

ADVERTISEMENTS: In this article we will discuss about the Regulation and Renal Threshold for Blood Glucose. Regulation of the Blood Glucose: The stable blood glucose level is maintained by the role of liver, skeletal muscle, kidney, muscular exercise and hormones. Role of Liver: 1. Liver is the pivot of carbohydrate metabolism of the whole body. The presence of glucose-6-phosphatase in the liver converts glucose-6-phosphate to glucose which diffuses into the blood stream to form the constant and the only source of glucose of blood unless and until glucose is available from the intestine from carbohydrate diet. 2. Muscle glycogen cannot be converted to glucose due to the lack of the enzyme glucose-6-phosphatase. Therefore, glycogen is converted to lactic acid which by “Cori Cycle” or “Lactic Acid Cycle” is converted to glucose in the liver and the glucose is diffused to the blood stream. 3. The liver cells, like other cells, require the oxidation of organic substances to maintain their own vital functioning. In the absence of fuel glucose, glycogen is diminished and the oxidation of fat occurs forming keto acids. Some of the keto acids are utilized for cellular energy. But if the concentration of keto acids is increased, the keto acids diffuse into the blood stream and accumulate producing ketosis. 4. When the glycogen reservoir diminishes, the amino acids of the body proteins are utilized by the liver for gluconeogenesis. Role of Skeletal Muscle: 1. Extra-hepatic tissues are relatively impermeable to glucose and, therefore, insulin is required for the uptake of glucose to these cells. 2. Increased blood glucose promotes glycogenesis and oxidation of glucose in muscles. Muscle glycogen does not serve directly as a source of glucose during hypoglycemia. But glucos Continue reading >>

Inhibition Of Renal Glucose Reabsorption As A Novel Treatment For Diabetes Patients

Inhibition Of Renal Glucose Reabsorption As A Novel Treatment For Diabetes Patients

The importance of the kidney in glucose homeostasis has been recognized for many years. Recent observations indicating a greater role of renal glucose metabolism in various physiologic and pathologic conditions have rekindled the interest in renal glucose handling as a potential target for the treatment of diabetes. The enormous capacity of the proximal tubular cells to reabsorb the filtered glucose load entirely, utilizing the sodium-glucose co-transporter system (primarily SGLT-2), became the focus of attention. Original studies conducted in experimental animals with the nonspecific SGLT inhibitor phlorizin showed that hyperglycemia after pancreatectomy decreased as a result of forced glycosuria. Subsequently, several compounds with more selective SGLT-2 inhibition properties (second-generation) were developed. Some agents made it into pre-clinical and clinical trials and a few have already been approved for commercial use in the treatment of type 2 diabetes. In general, a 6-month period of therapy with SGLT-2 inhibitors is followed by a mean urinary glucose excretion rate of ~80 g/day accompanied by a decline in fasting and postprandial glucose with average decreases in HgA1C ~1.0%. Concomitant body weight loss and a mild but consistent drop in blood pressure also have been reported. In contrast, transient polyuria, thirst with dehydration and occasional hypotension have been described early in the treatment. In addition, a significant increase in the occurrence of uro-genital infections, particularly in women has been documented with the use of SGLT-2 inhibitors. Although long-term cardiovascular, renal and bone/mineral effects are unknown SGLT-2 inhibitors, if used with caution and in the proper patient provide a unique insulin-independent therapeutic option in th Continue reading >>

Effect Of Canagliflozin On Renal Threshold For Glucose, Glycemia, And Body Weight In Normal And Diabetic Animal Models

Effect Of Canagliflozin On Renal Threshold For Glucose, Glycemia, And Body Weight In Normal And Diabetic Animal Models

Click through the PLOS taxonomy to find articles in your field. For more information about PLOS Subject Areas, click here . Effect of Canagliflozin on Renal Threshold for Glucose, Glycemia, and Body Weight in Normal and Diabetic Animal Models Affiliation Johnson & Johnson Pharmaceutical Research & Development, LLC, Spring House, Pennsylvania, United States of America Affiliation Pharmacology Laboratory, Mitsubishi Tanabe Pharma Corporation, Toda, Saitama, Japan Affiliation Pharmacology Laboratory, Mitsubishi Tanabe Pharma Corporation, Toda, Saitama, Japan Affiliation Pharmacology Laboratory, Mitsubishi Tanabe Pharma Corporation, Toda, Saitama, Japan Affiliation Pharmacology Laboratory, Mitsubishi Tanabe Pharma Corporation, Toda, Saitama, Japan Affiliation Johnson & Johnson Pharmaceutical Research & Development, LLC, Spring House, Pennsylvania, United States of America Affiliation Johnson & Johnson Pharmaceutical Research & Development, LLC, Spring House, Pennsylvania, United States of America Affiliation Johnson & Johnson Pharmaceutical Research & Development, LLC, La Jolla, California, United States of America Affiliation Johnson & Johnson Pharmaceutical Research & Development, LLC, Spring House, Pennsylvania, United States of America Affiliation Johnson & Johnson Pharmaceutical Research & Development, LLC, Spring House, Pennsylvania, United States of America Affiliation Johnson & Johnson Pharmaceutical Research & Development, LLC, Spring House, Pennsylvania, United States of America Affiliation Johnson & Johnson Pharmaceutical Research & Development, LLC, La Jolla, California, United States of America Affiliation Johnson & Johnson Pharmaceutical Research & Development, LLC, Raritan, New Jersey, United States of America Continue reading >>

Renal Glucose Handling In Diabetes And Sodium Glucose Cotransporter 2 Inhibition Poudel Rr - Indian J Endocr Metab

Renal Glucose Handling In Diabetes And Sodium Glucose Cotransporter 2 Inhibition Poudel Rr - Indian J Endocr Metab

Diabetes has prevailed through many civilizations as a devastating and deadly disease before the discovery of insulin and still an incurable disease. Insulin resistance in muscles, liver and adipose tissue has been long considered as the fundamental pathology in type 2 diabetes mellitus (T2DM). [1] Besides the contribution of kidney in glucose homeostasis through gluconeogenesis and glucose utilization, abnormal renal glucose reabsorption is yet another key abnormality in pathogenesis of T2DM, defined as the septicidal septet in the ominous octet by Ralph. DeFronzo in his Banting Lecture. The other seven players in the ominous octet are muscle, liver, fat cells, pancreatic -cells, pancreatic -cells, gastrointestinal tract, and brain. [2] The sodium glucose cotransporter (SGLT) 2 and SGLT1 are the sites of reclamation of all the filtered glucose, which are maladaptive in the kidneys of type 2 diabetics. SGLT2 inhibitors are the emerging treatment targeting this defective renal glucose reabsorption. [3] , [4] The major role of kidney in human physiology is to maintain intravascular volume and acid-base and electrolyte balance through filtration, secretion and selective reabsorption of vital minerals sodium, potassium, and chloride; hydrogen and bicarbonate ions. Glucose is also filtered and reabsorbed in similar fashion in order to retain energy essential for physiological functioning between meals. With a daily glomerular filtration rate of 180 L, approximately 162 g (180 L/day 90 mg/dL) of glucose must be reabsorbed each day to maintain a normal fasting plasma glucose concentration of 5.6 mmol/L (101 mg/dL). Reabsorption of glucose occurs mainly in the proximal tubule and is mediated by 2 different transport proteins, SGLT1 and SGLT2. SGLT1, which are found in the stra Continue reading >>

Impaired Decline In Renal Threshold For Glucose During Pregnancy - A Possiblenovel Mechanism For Gestational Diabetes Mellitus.

Impaired Decline In Renal Threshold For Glucose During Pregnancy - A Possiblenovel Mechanism For Gestational Diabetes Mellitus.

1. Diabetes Metab Res Rev. 2014 Feb;30(2):140-5. doi: 10.1002/dmrr.2474. Impaired decline in renal threshold for glucose during pregnancy - a possiblenovel mechanism for gestational diabetes mellitus. Klein P(1), Polidori D, Twito O, Jaffe A. (1)Diabetes and Endocrinology Unit, Hillel Yaffe Medical Center, Hadera, Israel. BACKGROUND: The renal threshold for glucose (RT(G)) is determined by thenephron's reabsorptive capacity. Glucose is reabsorbed through sodium-coupledglucose cotransporters in the proximal tubules. During pregnancy, renal glucosereabsorptive capacity decreases, possibly, due to reduced glucose transporterexpression. Our hypothesis is that inadequate decrease in RT(G) during pregnancy will make women more prone to develop gestational diabetes mellitus (GDM).METHODS: Pregnant women (n = 40) who were referred to our center for oral glucosetolerance test (OGTT) were included in the analysis. Plasma glucose levels andurinary glucose excretion were measured for 4 h after 100 g oral glucose load.These data were used to calculate RT(G) . The subjects were divided into twocohorts, GDM and non-GDM, according to the OGTT results. Mean RT(G) was compared between the two groups.RESULTS: Fifteen (37.5%) of the women were diagnosed with GDM. Seventeenparticipants had only trace amounts of urinary glucose excretion, and no value ofRT(G) could be determined; RT(G) was determined in the other 23 subjects. Amongthese 23 women, 13 were diagnosed as GDM, and 10 had normal OGTT. RT(G) was lowerin the non-GDM women (146 14 mg/dL) than in the GDM women (182 18 mg/dL),p < 0.001.CONCLUSIONS: Gestational diabetes mellitus is associated with higher RT(G) duringpregnancy compared with non-GDM. These results support our hypothesis thatinadequate decrease of the RT(G) may have a pat Continue reading >>

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