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PubMed1993

Perimenstrual symptoms in women with diabetes mellitus and the relationship to diabetic control.

Four hundred and six insulin-dependent diabetic women completed a Menstrual Health Questionnaire published in Balance. Sixty-seven percent of women experienced changes in blood glucose levels or glycosuria premenstrually and 70% during the menstrual phase. Changes were more common in women who regarded themselves as suffering from premenstrual syndrome. Those experiencing premenstrual craving for sweet foods tended to have higher blood glucose levels or more glycosuria at those times. This may be a consequence of some women indulging their craving. Premenstrual symptoms were not caused by hypoglycaemia. When compared with age-matched non-diabetic women responding to a similar questionnaire, the diabetic women had a later menarche and, among those not on steroidal contraceptives, were more likely to report very irregular menstrual cycles. Among those regarding themselves as sufferers of premenstrual syndrome, diabetic women had less severe premenstrual symptoms than non-diabetic women. When women from these two self-designated premenstrual [corrected] syndrome suffering groups were matched for severity of premenstrual depression, differences still persisted in the severity of some symptoms perimenstrually, raising the possibility that in some way diabetes may alter women's experience of menstrual cycle-related symptoms.

Adolescent↗

PubMed1990

Effects of self-monitoring of blood glucose on quality of life in elderly diabetic patients.

Self-monitoring of blood glucose (SMBG) has been associated with improvement in diabetes knowledge and glycemic control in young and middle-aged diabetic patients. This study investigated the influences of SMBG on the quality of life in 20 older diabetic individuals, aged 60 to 79 years with duration of diabetes 15.6 +/- 2.3 (SD) years. Questionnaires (Cronbach's alpha reliability = .93) were administered regarding the impact of four aspects of diabetic self-care--general factors, diet, medications, and monitoring blood or urine--on quality of life. Each category was scored separately. Data were analyzed comparing individuals using SMBG with those monitoring glycosuria. Older patients showed acceptance of SMBG with respect to performance, lack of time consumption, ease of record keeping, and less embarrassment. Individuals performing SMBG reported better medication compliance than those monitoring glycosuria. No differences were observed between the two groups for general factors, diet, or the overall perception of quality of life. Both groups of patients reported that diabetes and performing self-care techniques did not significantly interfere with their life-style. In conclusion, this study demonstrates that self-care techniques, such as SMBG, do not negatively influence the perception of quality of life in older people.

Aged↗

PubMed1999

Renal processing of glucose in well and sick neonates.

AIMS: To determine the extent of renal processing of glucose in sick and well neonates. METHODS: Glomerular filtration rate (GFR) and the renal processing of glucose, sodium, and water were measured using prolonged inulin infusion in 47 infants of 26-40 weeks of gestation, aged 1-13 days. RESULTS: GFR rose by 15% after ventilatory support was withdrawn, and was unaffected by clinical instability. Fractional glucose excretion was low in the stable unventilated babies except at very high filtered loads, but rose in one unstable, unventilated baby. It was higher in ventilated babies, and remained high for at least six days after ventilation. For water and sodium, net differences between intake and urine excretion were not affected by ventilation, clinical stability, or glycosuria. CONCLUSIONS: A combination of a low GFR and a high fluid intake, urine flow, and urine concentrating capacity, makes neonates very unlikely to develop an osmotic diuresis due to glycosuria while they have a blood glucose below 12 mmol/l, despite assertions to the contrary.

Analysis of Variance↗

PubMed1997

Role of the kidney in plasma glucose regulation during hyperglycemia.

Little is known about the role of the kidney in plasma glucose regulation during hyperglycemia. We studied 12 overnight-fasted conscious dogs after either intrarenal (IR, n = 6) or peripheral (PH, n = 6) dextrose infusion to maintain hyperglycemia without glycosuria. Systemic and renal glucose kinetics were measured with [6-3H]glucose, lactate balance was measured by arteriovenous difference, and glycogen content was assayed in the kidneys. Plasma glucose (approximately 5.5 vs. approximately 6.3 mM), insulin (approximately 70 vs. approximately 110 pM), and glucose appearance (approximately 14 vs. approximately 16 mumol.kg-1.min-1 increased comparably in both groups (P < 0.05). In IR, fractional extraction of glucose (FEGlc) increased from 4.1 +/- 0.2 to 16.1 +/- 0.5% (P < 0.001) and lactate balance reversed to renal output (+1.3 +/- 0.2 vs. -0.9 +/- 0.2 mumol.kg-1.min-1, P < 0.01). Glycogen content was twofold higher in the left (127 +/- 33 micrograms/g tissue) than in the right kidney (56 +/- 11 micrograms/g tissue, P < 0.01). In PH, FEGlc decreased from 4.9 +/- 0.6 to 2.2 +/- 0.3% (P < 0.05), renal glucose utilization did not change (approximately 1.3 mumol.kg-1.min-1); and glycogen content was equal in both kidneys (approximately 45 micrograms/g tissue). We conclude that, although the kidney plays a minor role in plasma glucose disposal in physiological hyperglycemia, increased glucose uptake, glycogen storage, and lactate formation precede glycosuria and may represent important mechanisms by which the kidney contributes to normalization of plasma glucose in diabetes.

Animals↗

PubMed2005

Urinary kidney injury molecule-1: a sensitive quantitative biomarker for early detection of kidney tubular injury.

Sensitive and specific biomarkers are needed to detect early kidney injury. The objective of the present work was to develop a sensitive quantitative urinary test to identify renal injury in the rodent to facilitate early assessment of pathophysiological influences and drug toxicity. Two mouse monoclonal antibodies were made against the purified ectodomain of kidney injury molecule-1 (Kim-1), and these were used to construct a sandwich Kim-1 ELISA. The assay range of this ELISA was 50 pg/ml to 5 ng/ml, with inter- and intra-assay variability of <10%. Urine samples were collected from rats treated with one of three doses of cisplatin (2.5, 5, or 7.5 mg/kg). At one day after each of the doses, there was an approximately three- to fivefold increase in the urine Kim-1 ectodomain, whereas other routinely used biomarkers measured in this study [plasma creatinine, blood urea nitrogen (BUN), urinary N-acetyl-beta-glucosaminidase (NAG), glycosuria, proteinuria] lacked the sensitivity to show any sign of renal damage at this time point. When rats were subjected to increasing periods (10, 20, 30, or 45 min) of bilateral ischemia, there was an increasing amount of urinary Kim-1 detected. After only 10 min of bilateral ischemia, Kim-1 levels on day 1 were 10-fold higher (5 ng/ml) than control levels, whereas plasma creatinine and BUN were not increased and there was no glycosuria, increased proteinuria, or increased urinary NAG levels. Thus urinary Kim-1 levels serve as a noninvasive, rapid, sensitive, reproducible, and potentially high-throughput method to detect early kidney injury in pathophysiological studies and in preclinical drug development studies for risk-benefit profiling of pharmaceutical agents.

Animals↗

PubMed1988

Effects of maternal hyperglycemia on fetal renal function in sheep.

The effects of maternal hyperglycemia on fetal renal function were investigated in 10 chronically catheterized fetal sheep after the infusion of 100 g of glucose into the ewe over 30 min. Fetal blood glucose levels rose (P less than 0.001) within 15 min of completing the glucose infusion from 15.75 +/- 2.8 to 195.4 +/- 18 (SE) mg/dl (n = 10). There was a significant increase in fetal glomerular filtration rate (P less than 0.05) from 2.73 +/- 0.41 to 3.65 +/- 0.40 (SE) ml/min (n = 10) within 1.5 h of the infusion of glucose into the ewe. Urine flow rate increased from 0.38 +/- 0.06 to 0.63 +/- 0.12 (SE) ml/min (n = 10, P less than 0.001), and sodium excretion increased from 18.42 +/- 7.21 to 38.4 +/- 13.7 (SE) mumol/min (n = 10, P less than 0.002) within 2.5 h of the infusion of glucose into the ewe. The fraction of the filtered load that was excreted (urine flow rate divided by glomerular filtration rate) also increased (P less than 0.01) as did the fraction of the osmolar load (P less than 0.002). Glycosuria occurred in all fetuses within 30 min of the infusion of glucose into the ewe, and glucose excretion reached 26.16 +/- 12.36 (SE) micrograms/min (n = 8) after 1.5 h. These findings of diuresis, natriuresis, and glycosuria in response to hyperglycemia are evidence that an increased delivery of fluid into the amniotic cavity might occur after a rise in fetal plasma glucose levels.

Animals↗

PubMed1988

Reversal of proteinuria by sorbinil, an aldose reductase inhibitor in spontaneously diabetic (BB) rats.

Sorbinil, an aldose reductase inhibitor, was examined as a therapeutic agent to arrest and/or reverse proteinuria in 'type 1' insulin-dependent BB rats having spontaneous diabetes mellitus. Prior to sorbinil treatment, diabetic rats exhibited hyperglycemia and increased urinary excretion of urobilinogen, glucose and protein. To assess proteinuria, 24-hour urine samples were analyzed for both total protein and individual components between 30,000 and 100,000 daltons. Daily oral administration of sorbinil (20 mg/kg body weight) was initiated and the aforementioned parameters reevaluated after 1, 2 and 4 months. Results indicated that after 1 month of sorbinil treatment, urobilinogen was normalized in all diabetic BB rats (n = 12), whereas urinary protein excretion was either diminished (67%) or remained constant (16%), despite persistence of hyperglycemia and glycosuria. These therapeutic effects were sustained after 2 months of sorbinil treatment. After 4 months, protein excretion was normalized (6.56 +/- 3.34 mg/24 h), despite persistence of hyperglycemia and glycosuria (n = 12); in marked contrast, 6 untreated rats continued to exhibit proteinuria (17.76 +/- 2.59 mg/day). Sorbinil diminished albumin and a series of urinary proteins between 30,000 and 100,000 daltons, suggesting that sorbinil may represent a therapeutic approach to manage diabetic nephropathy as indicated by diminution of proteinuria.

Aldehyde Reductase↗

PubMed1992

Comparison of sorbinil and ponalrestat (Statil) diminution of proteinuria in the BB rat.

Diabetic nephropathy leading to kidney failure is a major complication of type I (insulin-dependent) diabetes mellitus and is associated with progressive proteinuria. In the present 6-month study, effects of two structurally dissimilar aldose reductase inhibitors (sorbinil and ponalrestat or Statil) were examined on prevention of proteinuria in insulin-dependent spontaneously diabetic BB rats and compared with age-matched BB resistant controls. Prior to aldose reductase inhibitor treatment, all diabetic BB rats exhibited hyperglycemia (> 300 mg/dl), glycosuria (> 2,000 mg/dl) and 24-hour urinary protein excretion ranging from 5.01 to 11.23 mg/day. After daily administration of ponalrestat (20 mg/kg) for 3 months, 24-hour urinary protein excretion was 11.53 +/- 1.76 mg/day in ponalrestat-treated rats, despite persistence of hyperglycemia (444 +/- 31 mg/dl) and glycosuria (> 2,000 mg/dl); by contrast, urinary protein excretion was 17.76 +/- 2.59 mg/day in the control group of untreated BB diabetic rats. Ponalrestat initially protected against excretion of an array of urinary proteins having molecular weights between 30,000 and 100,000 daltons. These effects sustained throughout the 4th month of treatment, tended to change toward valves in control rats by the 5th month. At the end of 6 months, ponalrestat-treated diabetic rats excreted 18.73 +/- 3.20 mg/day of protein, similar to valves in untreated BB diabetic rats; both demonstrated a 4-fold increase in urinary protein excretion when compared to age-matched BB resistant controls. Proteinuria was attributed to an increase in albumin and an array of proteins having molecular weights between 30,000 and 100,000 daltons.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1990

Sodium excretion and hyperfiltration during glucose infusion in man.

The relations between renal hemodynamics (Inutest, CPAH) and sodium excretion were studied in 7 nondiabetics in whom a similar expansion was induced (1) with a 3-hour 5% glucose infusion and (2) with a 0.9% saline load. With both infusions the body weight increased, hematocrit fell, and the plasma renin activity was suppressed. During glucose infusion, blood glucose rose from 3.9 mmol/l to a plateau of around 13 mmol/l; glycosuria was absent during the 1st h, then appeared and stabilized during the following 2h. Glucose infusion caused a progressive increase in glomerular filtration rate and in renal blood flow in both absence and presence of glycosuria, without significant changes in sodium excretion despite volume expansion and increase of filtered sodium load. When saline was infused, there was a sustained increase of fractional sodium excretion, and no hemodynamic modifications were observed. We suggest that a primary glucose-induced metabolic stimulation of sodium reabsorption may play a role in the genesis of glucose-induced hyperfiltration.

Adolescent↗

PubMed1995

Effect of glucose infusion on the renal transport of purine bases and oxypurinol.

The effect of glucose infusion on renal handling of purine bases and oxypurinol was examined in 6 normal subjects. Five hundred milliliters of 1.1 M glucose solution were administered intravenously in 1 h. Fractional clearances of uric acid, xanthine and oxypurinol were significantly increased during glucose infusion, but that of hypoxanthine was not changed, while a 1-hour infusion of 500 ml of 1.1 M mannitol had no effect on the fractional clearances of purine bases and oxypurinol. These data indicate that the effect of glucose infusion on the renal clearances of uric acid, xanthine and oxypurinol was not related to osmotic diuresis but induced by glycosuria and/or hyperglycemia. Accordingly, the glycosuria- and/or hyperglycemia-induced decrease in the biological half-life of oxypurinol must be considered in the administration of allopurinol to gouty patients with uncontrolled diabetes mellitus.

Adult↗

PubMed1976

Membrane permeability as a cause of transport defects in experimental Fanconi syndrome. A new hypothesis.

The injection of sodium maleate (200-400 mg/kg) into rats produces aminoaciduria along with glycosuria and phosphaturia, resembling the Fanconi syndrome. This experimental model was studied by means of microinjections into proximal convoluted tubules of the kidney, stop-flow diuresis, and microperfusion of single nephrons. Our results show that, in maleate-treated rats, competition between amino acids or related structures (L-proline, L-OH-proline, and glycine) possesses the same characteristics, and net influx of amino acids appear normal at the proximal nephron. Data obtained by classical stop-flow techniques and single nephron microperfusions also indicate a normal entry of labeled amino acids (L-lysine, glycine, L-valine, L-proline, L-cystine), and 3-0-methyl-D-[3H]glucose and [32P]phosphate from the luminal side of the proximal tubule cell. However, the efflux of molecules from the cell appears enhanced throughout the proximal and distal tubule; molecules that exit at this site are excreted directly into the urine. Our results suggest that the phosphaturia, aminoaciduria, and glycosuria of the experimental Fanconi syndrome can be explained by a modification of the cell membrane permeability (increased efflux) at distal sites of the nephron rather than by a modification of the membrane transport (decreased influx) at the proximal sites, as is currently accepted. Our data also stress the importance of efflux phenomena in membrane transport.

Amino Acids↗

PubMed1978

Effect of oral glucose ingestion on renal phosphate reabsorption and clearance in vitamin D-resistant rickets.

The effect or oral glucose ingestion on renal phosphate reabsorption was studied in 13 patients with the inherited form of vitamin D-resistant rickets (VDRR) and 5 normal subjects. In contrast to the normal subjects, glycosuria developed in six VDRR patients after glucose ingestion and resulted in a further 43% decrease in renal phosphate reabsorption. This was accompanied by a 33% increase in phosphate clearance. This was not attended by differences in fasting glucose or phosphorus levels between groups, or in their respective values 1 h after glucose ingestion. Baseline renal phosphate reabsorption was less and baseline phosphate clearance was greater in those VDRR subjects who developed glycosuria. The accumulated data suggest that excessive glucose ingestion by some patients with VDRR may add an additional insult to the phosphaturia characteristic of this disorder. This, in turn, would further compromise the response of circulating phosphate to therapeutic attempts at oral phosphate supplementation, thereby reducing the efficacy of oral phosphate therapy on skeletal growth and development in this disorder.

Adolescent↗

PubMedDate not supplied

Hypophosphataemic osteomalacia due to de Toni-Debre-Fanconi syndrome in a 19-year old girl.

Osteomalacia associated with adult onset Fanconi syndrome is thought to result from hypophosphataemia due to renal phosphate loss and relative 1,25-dihydroxyvitamin D3 deficiency. In this disorder, the impaired renal phosphate uptake occurs as part of a generalized tubular defect in association with other features such as bicarbonuria, glycosuria and aminoaciduria. Fanconi syndrome is either hereditary--juvenile form--or is associated with various acquired or heritable diseases. In adults, the disease is similar to the juvenile form, but osteomalacia is a prominent feature. We report a sporadic, adult onset, hypophosphataemia in a 19-year old female patient who presented after puberty complaining of bone and joint pain and difficulty in walking following a minor fall. Radiological examination revealed numerous bilateral fractures of the ribs and pelvis while biochemical investigations showed combination of high phosphate clearance, low serum bicarbonate, glycosuria and glycinuria. Known causes of acquired renal tubular dysfunction were ruled out. The patient was diagnosed as having idiopathic Fanconi syndrome and started on vitamin D3 (Alfacalcidol 1 mg/day) and oral phosphorus (Joulie Solution, 1.5 g/day), which led to resolution of symptoms and an increase in serum phosphate (from 0,54 to 0,71 mmol/l) within few months following the initiation of therapy. However, radiological re-examination showed no signs of fracture healing.

Adult↗

PubMed1979

Bone mineral loss in insulin-treated diabetes mellitus: studies on pathogenesis.

To elucidate pathogenetic factors of bone mineral loss in diabetes mellitus, bone mineral content (BMC), glucose and calcium homeostasis were evaluated in a cross-sectionsl study of 215 insulin-treated diabetics. BMC declined 10% during the first 5 years of diabetes. This coincided with cessation of insulin secretion, deterioration of metabolic control and raising urinary calcium excretion rates of calcium and phosphorus. BMC was inversely correlated to fasting blood glucose (P less than 0.02), to glycosuria (P less than 0.02) and to insulin requirement (P less than 0.002), and positively to the glucagon-stimulated serum C-peptide levels (P less than 0.005). Urinary excretion rates of calcium and phosphorus correlated positively with the degree of hyperglycaemia (P less than 0.001) and glycosuria (P less than 0.001). The skeletal calcium loss corresponded to the excess of urinary excretion during the phase of BMC reduction. There was no evidence of secondary hyperparathyroidism. The relationship between bone loss and disturbed glucose homeostasis indicates that diabetic bone loss is secondary to the metabolic abnormalities, possibly acting directly on bone.

Adolescent↗

PubMed1997

Renal hypertrophy in hyperglycemic non-obese diabetic mice is associated with persistent renal accumulation of insulin-like growth factor I.

The non-obese diabetic mouse is a model of spontaneous insulin-dependent diabetes as a result of autoimmune destruction of pancreatic beta cells, similar to the disease seen in human Type I diabetes. This mouse strain develops glomerular lesions reminiscent of those seen in human disease. The study presented here investigated the changes in renal insulin-like growth factor (IGF) system in hyperglycemic non-obese diabetic mice. Female non-obese diabetic mice and their age- and sex-matched controls were euthanized 4 days, 2 wk, and 4 wk after the onset of glycosuria. Kidney weight increased in diabetic mice, beginning at 2 wk after the onset of glycosuria. This renal hypertrophy was associated with an increase in renal extractable IGF-I protein. However, a decrease in IGF-I mRNA was observed at the same time. Serum IGF-I levels remained stable after 2 wk of diabetes and decreased at 1 month. No change was detected in renal IGF-I receptor mRNA levels. Renal cortical IGF binding protein (IGFBP)-1 mRNA levels were increased. Ligand blot analysis revealed a significant increase in serum and renal 30-kd IGFBP and a decrease in serum and kidney IGFBP-3 and IGFBP-4 at 30 days of diabetes. Insulin therapy prevented the increases in kidney weight, renal IGF-I, and 30-kd IGFBP, but did not reverse the decreased serum IGF-I levels observed at 1 month of diabetes. In summary, renal hypertrophy in non-obese diabetic mice is associated with a persistent accumulation of renal IGF-I and, IGFBP-1. These changes were partially reversed with insulin therapy, which did not correct the hyperglycemia, suggesting an important role for insulin deficiency in mediating these changes in the IGF system. These findings suggest that the IGF system may play a potential role in the development of diabetic nephropathy.

Animals↗

PubMed1991

Cardiovascular risk factor levels in ethnic Hawaiians.

We report a cardiovascular risk factor survey of "native" Hawaiians 20-59 years old (70 percent, or 257), living on the Hawaiian Homestead lands on the island of Molokai, Hawaii. More than 60 percent of both sexes were overweight. Among males, 42 percent were smokers. The percent of the population with systolic blood pressure greater than 140 mm Hg or a diastolic pressure greater than 90 mm Hg or taking hypertensive medications was 14 percent of those ages 20-39 and 36 percent of those ages 40-59. The percent with serum cholesterol greater than or equal to 6.2 mmol/L ranged from 8 percent of those 20-29 years old to 46 percent in those 50-59 years old. Two percent of those ages 20-29 had a history of diabetes, or 2 + or greater glycosuria by dipstick, as did 23 percent of those ages 50-59. The majority of the known diabetics exhibited glycosuria and elevated glycohemoglobin levels, indicating poor control. Hypertension, although usually known to the participant, was frequently uncontrolled. From these data, it appears that among this group of Hawaiians major risk factors for cardiovascular disease were frequent, while at the same time the levels of awareness and/or control for most of these factors were low.

Adult↗

PubMed1982

The Chinese hamster as a model for the study of diabetes mellitus.

Selection for and against diabetes and subsequent inbreeding of Chinese hamsters started in 1963. Currently there are six inbred sublines that have greater than 85% incidence of glycosuria and two control inbred nondiabetic sublines that are essentially free of glycosuria. At birth, hamsters from inbred sublines are considered prediabetic. There is phenotypic variation between diabetic sublines. Onset time, incidence of ketonuria, blood glucose, plasma insulin, glucagon and glycohydrolase levels vary from subline to subline, but pancreatic insulin and glucagon levels are consistently low and high, respectively, in all diabetic sublines compared with nondiabetics. Experimental breeding data suggest a minimum of two homozygous recessive genes for diabetes. It is not known if the inbred lines are similar diabetic genotypes, but the probability is high that modifier background genes vary from subline to subline. Chinese hamsters have diabetes ranging from mild to severe. Animals weighing 25 g can excrete up to 75 ml of urine containing 3 g of glucose per day. Fasting blood glucose as high as 500 mg/dl and 10 mumol/ml of beta-hydroxybutyrate have been reported. Gluconeogenesis is elevated, and some glycolytic enzymes are decreased in severe diabetes. Low levels of renal acid glycohydrolase enzymes may contribute to glomerular capillary loop basement membrane thickening in diabetic hamsters. Caloric restriction per se or reduction of dietary fat prevented onset of hyperglycemia and hyperinsulinemia in prediabetics. Morphologic changes have been observed in pancreatic islets, kidney, nerve, blood vessels, eyes, brain, and genito-urinary systems of diabetic Chinese hamsters. Pathogenesis of diabetes in this animal appears to be related to an increased demand for insulin. Initially there is a positive response to this demand by beta cells, but exhaustion occurs. This is followed by a decrease in beta-cell mass and relative or absolute insulin deficiency.

Animals↗

PubMed1993

Intensive insulin therapy and weight gain in IDDM.

Intensive insulin therapy is frequently complicated by excessive weight gain. The purpose of this study was to determine the cause and composition of this weight gain. Therefore, changes in body composition, energy expenditure, glycosuria, and substrate kinetics were evaluated in patients with IDDM who transferred from conventional insulin therapy to intensive insulin therapy. Six adult patients with IDDM were studied on conventional insulin therapy and after 2 mo of intensive insulin therapy while maintaining constant caloric intake and were compared with a group of 6 matched nondiabetic volunteers. Body composition was determined by underwater weighing. Energy expenditure was measured during 24-h stays in a whole-room calorimeter. Whole-body turnover rates of glucose, glycerol, palmitate, and leucine were determined by isotope dilution methods. Intensive insulin therapy lowered the mean daily blood glucose concentration and HbA1 (14.8 +/- 1.6 to 7.7 +/- 0.6 mM and 12.9 +/- 0.9 to 9.6 +/- 0.6%, both P < 0.01) and almost eliminated glycosuria (428 +/- 116 to 39 +/- 22 mmol/day, P < 0.05). Body weight increased 2.6 +/- 0.8 kg with intensive insulin therapy (P < 0.05) as a result of an increase in fat mass (2.4 +/- 0.8 kg, P < 0.05). Daily energy expenditure decreased 5% (118 +/- 32 kcal/day) with intensive insulin therapy (P < 0.05). The rates of glucose, glycerol, free fatty acid, and leucine turnover, triglyceride/free fatty acid cycling, and nonoxidative glucose and protein disposal were reduced in the diabetic volunteers during intensive insulin therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗