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Biomedical subjects

D T Finegood

Publications and source records attributed to D T Finegood.

At least 37 records · Page 2Linked to original sources
PubMed1997

Apoptosis participates in the remodeling of the endocrine pancreas in the neonatal rat.

In rodents, shortly after birth a lack of increase in pancreatic weight and in islet mass have been reported during a time of overall body weight increase. To understand this regulation of the neonatal growth of the beta cell mass, we studied Sprague Dawley rats at 2, 9, 13, 17, 20, 24, and 31 days of age for beta cell replication, beta cell mass, and cell size and for the presence of cell apoptosis. beta cell mass was stable from 2-20 days (range: 0.91 +/- 0.2 to 1.33 +/- 0.23 mg) and increased thereafter. beta cell replication progressively decreased. Condensed apoptotic nuclei were identified and counted on paraffin sections using the fluorescent dye propidium iodide. Apoptotic beta cell nuclei were found at a basal rate (1.54 +/- 0.22%) at 2, 9, and again after 20 days of age. However, at 13 and 17 days, the incidence of apoptosis was significantly increased (3.64 +/- 0.45%). The decreased replication and the increased incidence of apoptosis in the beta cells strongly suggest a wave of neogenesis of beta cells to maintain the constant beta cell mass. These data show that the endocrine pancreas undergoes significant modification during neonatal life and that apoptosis is an important mechanism in this remodeling of the beta cell mass. Whether a selective deletion of some population of beta cells occurs is unclear, but a dysregulation of this remodeling process could have important effects on the pancreatic beta cell mass.

Animals↗
PubMed1997

Factors affecting glucose tolerance in hereditary hemochromatosis.

OBJECTIVE: To determine insulin action and insulin secretory function in patients with hemochromatosis, and to find evidence for or against hypothesized pathogenetic mechanisms for the abnormal glucose metabolism associated with hemochromatosis. These mechanisms include decreased beta-cell secretion of insulin due to iron overload, insulin resistance and genetic factors. DESIGN: Prospective in vivo study. PARTICIPANTS: Seventeen subjects with hemochromatosis, of whom 4 had cirrhosis but not diabetes mellitus, 6 had diabetes mellitus and 7 had neither; 10 controls. INTERVENTIONS: Insulin sensitivity and insulin secretion were determined during an intravenous glucose tolerance test. Insulin secretion was measured as the acute insulin response to glucose (AIRg). Insulin sensitivity (Si) was quantified with the minimal-model method. Of the patients with hemochromatosis, 14 agreed to undergo a second metabolic study after treatment with venous phlebotomy. RESULTS: All subjects with hereditary hemochromatosis had impaired glucose tolerance as measured by K(g) (rate of glucose disappearance). Subjects who were free of both diabetes mellitus and liver cirrhosis had a normal S1 and a decreased AIRg. In these subjects, phlebotomy treatment normalized serum ferritin levels, increased AIRg by 35% and normalized glucose tolerance (K(g)). Subjects with hemochromatosis and cirrhosis had a reduced Si and maintained a normal insulin secretion. Phlebotomy treatment did not change these parameters. Subjects with hemochromatosis and diabetes mellitus had both a reduced Si and AIRg, and these parameters were unaffected by phlebotomy treatment. CONCLUSIONS: These results suggest that iron overload can impair insulin secretion and glucose tolerance early in hereditary hemochromatosis, before cirrhosis occurs. Phlebotomy treatment can reverse these defects. Impaired glucose tolerance resulting from insulin resistance in subjects with cirrhosis or diabetes mellitus is not affected by phlebotomy treatment.

Adult↗
PubMed1996

Consequences of high dietary fructose in the islet-transplanted rat with suboptimal beta-cell mass.

Fructose (FR) feeding in rats provides a model of dietary-induced insulin resistance that has been used to examine interactions among the cluster of metabolic disorders including insulin resistance, hyperinsulinemia, hypertension, and dyslipidemia known as Syndrome X. In animals with reduced beta-cell mass, however, insulin resistance may not have similar associated disorders. Therefore this study examined the consequences of FR feeding in rats with a reduced beta-cell mass. Formerly diabetic islet-transplanted (TX) or shamoperated (SHAM) male Wistar Furth rats were fed a purified control (CNTL) diet or a diet containing either 40 or 70% (wt/wt) FR for 3-5 wk. FR feeding in SHAM animals resulted in elevated triglyceride levels but did not affect fed or fasting glucose and insulin concentrations, blood pressure, glucose tolerance, and the acute insulin response to a glucose bolus compared with CNTL-fed animals. Among TX animals, hypertriglyceridemia and fasting hyperglycemia were observed only in those fed FR. Thus the effects of diet-induced insulin resistance are limited to dyslipidemia, if insulin secretory capacity is adequate, but are detrimental to both glucose and lipid metabolism in combination with a reduced beta-cell mass.

Animals↗
PubMed1996

Reduced glucose effectiveness associated with reduced insulin release: an artifact of the minimal-model method.

We previously demonstrated that minimal model-derived estimates of glucose effectiveness (SG), based on the frequently sampled intravenous glucose tolerance test (SGFSIGT), were reduced in islet-transplanted or streptozotocin-treated dogs and in patients with insulin-dependent diabetes mellitus. To ascertain the validity of our observations, we compared SGFSIGT with estimates based on a basal hormone replacement glucose clamp (SGBRCLAMP) and a basal hormone replacement glucose tolerance test (SGBRGTT) in normal control (CNTL, n = 12) and streptozotocin-treated dogs with normal fasting plasma glucose (STZ-Rx, n = 9). SGFSIGT was reduced in STZ-Rx compared with CNTL (P < 0.05). However, neither SGBRCLAMP nor SGBRGTT was reduced in the STZ-Rx group (P > 0.05). Comparison of protocols for each subject indicated that SGFSIGT was greater than either SGBRCLAMP or SGBRGTT in control (P < 0.002) but not in STZ-Rx dogs (P > 0.1). The relationship of SGFSIGT to insulin secretory function suggests that our previous conclusion that SGFSIGT was reduced in subjects with limited insulin release may be an artifact of the minimal-model method. Our results suggest that caution must be exercised in the interpretation of differences in minimal-model estimates of SG between subject groups with significantly different levels of insulin secretory function.

Animals↗
PubMed1996

Beta-cell dysfunction independent of obesity and glucose intolerance in the polycystic ovary syndrome.

Several distinct groups of subjects at high risk to develop noninsulin-dependent diabetes mallitus (NIDDM) have been found to have insulin secretory defects when beta-cell function is assessed in the context of peripheral insulin sensitivity. We investigated this with a modified frequently sampled iv glucose tolerance test to determine acute insulin responses to glucose (AIRg) as well as insulin action by minimal model analysis in 28 women with polycystic ovary syndrome (PCOS; 15 obese and 13 nonobese) and 29 age- and weight-matched normal women (14 obese and 15 nonobese). No subject, PCOS or control, had fasting hyperglycemia, but seven PCOS women (six obese and one nonobese) had impaired glucose tolerance or NIDDM. The PCOS women had significantly decreased insulin sensitivity compared to the normal women (P < or = 0.001), and the obese women were less sensitive than the nonobese women (P < or = 0.001). The empiric measure of insulin release, AIRg, was significantly increased by obesity (P < or = 0.01), but not by PCOS. However, the disposition index (insulin sensitivity x AIRg) was significantly decreased by both PCOS (< or = 0.005) and obesity (< or = 0.005), suggesting that AIRg was inadequate for the degree of insulin resistance. When the PCOS women with impaired glucose tolerance or NIDDM were removed from the analysis, all of the reported PCOS-related changes in insulin action and secretion remained significant. We conclude that both obese and nonobese PCOS women have beta-cell dysfunction as well as insulin resistance. However, this was not associated with glucose intolerance in the majority of PCOS women.

Adult↗
PubMed1996

Long-term normalization of GLUT-4 protein content in skeletal muscle of diabetic rats following islet transplantation.

Skeletal muscle GLUT-4 content is decreased in streptozotocin (STZ)-diabetic rats. This decrease is associated with impairment in glucose transport across the plasma membrane. In this study we investigated whether islet transplantation might normalize GLUT-4 content. Transplantation of syngeneic islets restored long-term near-normoglycemia in STZ-diabetic Lewis rats. Transplanted rats, followed up to 6 months, maintained slightly but significantly higher fasting and fed glucose levels when compared with age-matched normal controls. Although fasting insulin levels of transplanted rats were significantly higher than those of controls, insulin levels did not increase significantly with feeding. Plasma glucose levels following an oral glucose load (2 g/kg) were only slightly higher than in normal controls 2 months after transplantation, whereas after 6 months more severe glucose intolerance was detected. Transplanted rats completely lost the first-phase insulin release in response to i.v. glucose although they showed an increased second phase and preserved response to arginine. Six months after transplantation, endocrine beta cell mass of the grafts was similar to pretransplantation values. GLUT-4 protein content in skeletal muscle homogenates was reduced in untreated diabetic animals whereas it was completely restored by islet transplantation. In conclusion, achievement of long-term nearnormoglycemia after islet transplantation was associated with complete normalization of skeletal muscle GLUT-4 content in the diabetic animals, even in the presence of abnormal glucose tolerance and an altered pattern of insulin secretion.

Animals↗
PubMed1996

A comparison of the effects of n-3 fatty acids from linseed oil and fish oil in well-controlled type II diabetes.

OBJECTIVE: Supplementation of type II diabetic diets with n-3 fatty acids (FAs) from fish oil (FO) has been associated with lowered triglyceride and VLDL levels, although reports of impaired glycemic control have limited their use. Effects of n-3FAs from nonmarine sources are less well documented. Therefore, an investigation comparing the effects of linseed oil (LO) with FO supplementation was undertaken in subjects with type II diabetes. RESEARCH DESIGN AND METHODS: Eleven subjects with type II diabetes were given supplements with LO and FO for 3 months each in a randomized double-blind crossover fashion after 3 months of olive oil placebo. Oils were given as 35 mg FA.kg body wt-1.day-1. After each 3-month period, fasting glucose and insulin levels, HbA1c, lipid profiles, insulin sensitivity (SI), glucose effectiveness (SG), and acute insulin response to glucose (AIRG) were evaluated. RESULTS: HbA1c and lipid values were within the normal range at randomization. Repeated measures analysis of variance testing found no significant differences in weight; fasting glucose and insulin levels; HbA1c; total, LDL, and HDL cholesterol levels; SI; SG; or AIRG with either active oil. FO was associated with significant reductions in triglycerides and a trend toward decreased SI. CONCLUSIONS: In a population with well-controlled type II diabetes, 3 months of FO but not LO resulted in lowered triglyceride levels. Neither LO nor FO significantly affected glycemic control, cholesterol values, SG, or insulin secretion, while a nonsignificant trend toward decreased insulin sensitivity was found with FO.

Blood Glucose↗
PubMed1996

Glycogen synthase polymorphism, insulin resistance and hypertension.

The A(2) allele of the human glycogen synthase gene may be associated with hypertension in diabetic and non-diabetic Finnish subjects. The prevalence of the A(2) allele was investigated in 64 non-diabetic hypertensive subjects with borderline hypertension or established hypertension. Ambulatory blood pressure was performed on all subjects. Insulin sensitivity index (S(I)) was determined in subjects with borderline hypertension. The DNA fragment containing the XBaI restriction site was amplified by the polymerase chain reaction, digested by the XBaI enzyme and compared by gel electrophoresis with a positive control from Finland. Mean age +/- SD for age, S(I) and ambulatory blood pressure were respectively: 39 +/- 10 yrs, 60 +/- 30 min(-1)(nmol/mL) and 132 +/- 7/ 83 +/- 6 mmHg. Sixteen of the subjects were insulin resistant as determined by S(I) <70.0 and they had significantly higher BP and BMI than insulin sensitive subjects. The A(2) allele of the glycogen synthase was not detected in any subject. This suggests that the relation between the XBaI polymorphism of the glycogen synthase gene, insulin resistance and elevated blood pressure may be restricted to a limited and genetically uniform Finnish population.

Adult↗
PubMed1996

Islet transplantation in diabetic Lewis rats--a comparison of the transplantation sites kidney and spleen capsule.

Animal studies have been used to investigate different transplantation (Tx) sites to find best conditions for Tx in humans. A few long-term experiments of comparisons of different Tx-sites have been published. Therefore the aim of our study was to compare islet grafts transplanted under the kidney capsule (KTx) of male Lewis rats with grafts transplanted under the spleen capsule (STx) and to observe these animals over a period of 6 months. Diabetes was induced by Streptozotocin and rats were each transplanted with 2000 syngeneic islets under the kidney respectively the spleen capsule. 2 weeks after Tx all animals were normoglycemic. Over the following 6 months nearly normal plasma glucose levels could be maintained in the KTx group whereas the STx animals already became diabetic after 3 months. An oral glucose load after 2 months showed slightly elevated plasma glucose levels in the KTx group which only gained statistical significance in a similar test after 6 months. In the STx group definitely impaired glucose tolerance already prevailed at 2 months. An i.v. glucose tolerance test performed 6 months after Tx showed a loss of first phase insulin release in both Tx groups but an increased second phase release and a preserved response to L-arginine compared to controls. Insulin content remained unchanged in the KTx group, but was markedly reduced in the STx group after 6 months. In conclusion we may say that KTx is able to establish near-normoglycemia in streptozotocin-diabetic Lewis rats which can be maintained over a long period of time despite abnormal glucose tolerance and impaired insulin secretion STx could normalize plasma glucose only up to 3 months showing early impairment of glucose and insulin regulation. If KTx has immunological or local advantages (islet vascularization, innervation) compared to STx with higher dispersion of islets in spleen and portal vascular system remains unclear.

Animals↗
PubMed1995

Insulin action in previously diabetic rats receiving graded numbers of islets of Langerhans.

We characterized insulin sensitivity in islet transplanted rats receiving from 500 to 3000 islets. Male Wistar Furth rats made previously diabetic with streptozotocin (55 mg/kg) were infused intraportally with islets of Langerhans (500 islets: n = 8; 1000: n = 6; 2000: n = 6; 3000: n = 5) from syngeneic donors and compared with sham-operated controls (n = 7). At four weeks after islet transplantation, fasting blood glucose was not significantly different between groups (500: 5.1 +/- 0.3; 1000: 4.8 +/- 0.3; 2000: 5.1 +/- 0.3; 3000: 4.6 +/- 0.1; control: 4.7 +/- 0.2 mM; P = 0.6146), and fasting plasma insulin was also not different (P = 0.28). The acute insulin response to glucose (0.3 g/kg i.v.) was correlated with islet equivalent mass (r = 0.63, P = 0.004; transplant rats only); islet transplant animals presented a range of acute insulin secretion from 3 to 90% of control values. Insulin action was measured in vivo in fasted, conscious animals during a hyperinsulinemic-euglycemic glucose clamp with insulin infused at 29 and 72 nmol/kg/min. Despite a wide range of islet mass and insulin secretory capacity, there was no significant difference in the glucose infusion rate between islet groups at either insulin level (P = 0.8211, P = 0.8021). There was also no difference in the glucose infusion rate normalized to the prevailing insulin level (P = 0.1638, P = 0.2302). Thus, our results demonstrate that the islet transplanted rat is consistent with other animal studies and human studies illustrating that a diminished insulin secretion does not necessarily precipitate insulin resistance.

Animals↗
PubMed1995

Splanchnic infusions of short chain fatty acids do not change insulin sensitivity of pigs.

Long-term ingestion of high fiber diets is associated with reduced glucose concentrations during fasting and improved glucose tolerance (KG) in humans. Our objective was to determine if the beneficial effects of fiber were attributable to increased production of short-chain fatty acid (SCFA) in the large intestine. Effects of SCFA on insulin sensitivity (SI), glucose effectiveness (SG), KG and baseline concentrations of glucose, insulin, glucagon and free fatty acids were examined in unfed 20-50 kg pigs (n = 6). Animals randomly received separate portal infusions (0.32 mL.min-1) of saline, acetic, propionic, and butyric acid solutions (0.01 mmol SCFA kg body weight-1.min-1) for 7-d periods. On d 7, somatostatin and tolbutamide modified frequently sampled intravenous glucose tolerance tests were performed. SI and SG were calculated using Bergman's Minimal-Model. KG was determined by regression of log glucose curve versus time. SI, SG and KG values did not differ among the treatments (P > 0.05). Baseline concentrations of glucose, insulin, glucagon and free fatty acids were unaffected by infusion treatment (P > 0.05). Our results suggest that SCFA delivery is not directly responsible for improvements in glucose metabolism observed with long-term ingestion of high fiber diets.

Acetates↗
PubMed1995

Estimation of rat body composition by means of electromagnetic scanning is altered by duration of anesthesia.

We determined the effect of anesthesia on estimation of fat-free mass and body fat in rats using electromagnetic scanning (EMS). Male Wistar Furth rats (n = 7, approximately 226 g) were injected with 66 mg/kg ketamine hydrochloride and 6.6 mg/kg xylazine intramuscular anesthesia. EMS measures were repeated every 4 min, up to 80 min post-anesthesia injection. From 4 to 44 min post-injection, the EMS signal and consequently the estimation of fat-free mass decreased from 198 +/- 5 to 180 +/- 5 g (mean +/- SD, P < 0.05). Conversely, the estimation of body fat increased by 63% during this period of anesthesia (12.9 +/- 2.9 vs. 21.1 +/- 2.6 g/100 g body wt, P < 0.05). In cohort animals (n = 6), body temperature and respiration rate declined following anesthesia (P < 0.05), and may have correspondingly suppressed EMS signal via reduced ion flux and/or muscular activity. In another study the effects of food deprivation, tail position, and anesthesia duration were demonstrated to alter estimation of fat-free mass (P = 0.0001), but these effects were not interactive (P > 0.05). Proximate analysis of body composition in cohort rats indicated that EMS predicted fat-free mass with a 3.5% error when estimated at 4 min post-anesthesia injection. Taken together, these data suggest that standardized EMS protocols should be adopted to account for effects of anesthesia, animal position and food deprivation. When manufacturer's equations are used, body composition should be measured immediately after induction of anesthesia. However, laboratories that choose to internally generate EMS regression equations with proximate analysis should determine and utilize the period of minimal variability in EMS measures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Long-term consequences in offspring of diabetes in pregnancy: studies with syngeneic islet-transplanted streptozotocin-diabetic rats.

To study the long-term effects of exposure to maternal hyperglycemia and insulin deficiency in utero, we used the syngeneic islet transplanted streptozotocin-diabetic rat model of diabetes in pregnancy and examined insulin secretion and action in 6-month-old offspring. Female rats were rendered diabetic with streptozotocin and then transplanted with 2500, 750, or 500 islets. Control animals were also studied, and one group whose islet transplants failed remained diabetic. During pregnancy, plasma glucose levels in the diabetic rats and the groups receiving 500 and 750 islets were 24.7 +/- 1.0, 15.3 +/- 1.4, and 7.9 +/- 0.5 mmol/liter, respectively, all significantly greater than the control value (5.6 +/- 0.3 mmol/liter; P < 0.05). The plasma glucose level in the 2500 islet group was 6.2 +/- 0.2 mmol/liter, which was not significantly higher than the control value. When the offspring were studied at 6 months, there was no significant difference between groups in either glucose or insulin levels after iv glucose, although acute insulin secretion tended to be higher in the offspring of the diabetic animals. A study of insulin action with the euglycemic clamp at two insulin levels showed that insulin sensitivity was reduced in the offspring of diabetic animals vs. controls (1.97 +/- 0.24 vs. 7.58 +/- 0.95 mumol/liter x 100/kg/min.pmol/liter; P < 0.05). Insulin sensitivity was also significantly reduced in the 2500, 750, and 500 islet group offspring (4.81 +/- 0.57, 4.82 +/- 0.64, and 4.01 +/- 0.63 mumol/liter x 100/kg/min.pmol/liter; P < 0.05) compared to that in the control. There were no differences in insulin sensitivity between male and female animals. In summary, animals displaying maternal insulin deficiency have offspring who are insulin resistant without any evidence of iv glucose intolerance or diminished insulin secretion.

Animals↗
PubMed1995

Parallel regulation of the local vascular and systemic metabolic effects of insulin.

Recent studies have focused on the link between the development of disordered vascular regulation (e.g. hypertension) and alteration in the effects of insulin to mediate glucose uptake. We and others have recently demonstrated that insulin is a potent vasodilator. Further, it has been suggested that impairment of insulin-mediated vasodilation may be an important contributing factor in the development of increased peripheral resistance. However, whether the local vascular effects of insulin correlate with its systemic glucose regulatory effects remains unclear. Therefore, we assessed both vascular sensitivity to insulin (using dorsal hand vein linear variable differential transformer techniques) and glucoregulatory sensitivity to insulin (using the minimal model technique applied to a frequently sampled iv glucose tolerance test) in 12 normotensive nondiabetic volunteers. In these subjects, metabolic sensitivity to insulin and venous sensitivity to insulin were highly correlated (r2 = 0.42; P = 0.02). Additionally, vascular sensitivity to insulin was inversely correlated with fasting C-peptide levels (r2 = 0.49; P = 0.02). Both systemic and vascular sensitivities to insulin were also highly correlated with body mass index. These studies demonstrate that the glucoregulatory effects of insulin are paralleled by its local vasodilating effects and continue to support this linkage as an important factor in the correlation between alterations in systemic sensitivity to insulin and the development of elevated peripheral resistance in hypertension and obesity.

Adult↗
PubMed1995

Dynamics of beta-cell mass in the growing rat pancreas. Estimation with a simple mathematical model.

The growth and development of the endocrine pancreas has been studied for many years, but questions remain concerning the regulation of the mass of insulin-producing beta-cells both in the normal growing pancreas and during the pathogenesis of diabetes. The homeostatic control of beta-cell mass in both normal and pathophysiological conditions is based on the balance of cell proliferation, cell growth, and cell death. To gain insight into the relative contribution of each of these dynamic processes, we first mathematically analyzed the data available on the components involved in the maintenance of beta-cell mass, including rates of replication, beta-cell volume, and the beta-cell mass itself, at various ages in normal Sprague-Dawley rats. Then these data were combined in a simple mass balance equation to construct a mathematical model of the dynamics of the beta-cell mass in the normal growing rat pancreas. Such a model has allowed us to infer the contributions of fluxes that cannot be measured, i.e., neogenesis and cell death, to the known mass of beta-cells. Another important contribution of this model is to raise unanswered questions concerning the control of the balance of cell death and cell renewal in the endocrine pancreas.

Aging↗
PubMed1995

Defects in insulin secretion and action in women with a history of gestational diabetes.

Gestational diabetes mellitus (GDM) is associated with defects in insulin secretion and insulin action, and women with a history of GDM carry a high risk for the development of non-insulin-dependent diabetes mellitus (NIDDM). Assessment of subjects with a history of GDM who are currently normoglycemic should help elucidate some of the underlying defects in insulin secretion or action in the evolution of NIDDM. We have studied 14 women with normal oral glucose tolerance who had a history of GDM. They were compared with a group of control subjects who were matched for both body mass index (BMI) and waist-to-hip ratio (WHR). All subjects underwent tests for the determination of oral glucose tolerance, ultradian oscillations in insulin secretion during a 28-h glucose infusion, insulin secretion in response to intravenous glucose, glucose disappearance after intravenous glucose (Kg), and insulin sensitivity (SI) as measured by the Bergman minimal model method. The BMI in the post-GDM women was similar to that in the control subjects (24.9 +/- 1.2 vs. 25.4 +/- 1.4 kg/m2, respectively), as was the WHR ratio (0.80 +/- 0.01 vs. 0.76 +/- 0.01, respectively). The post-GDM women were slightly older (35.2 +/- 0.9 vs. 32.1 +/- 1.4 years, P = 0.04). The fasting plasma glucose levels were significantly higher in the post-GDM group than in the control group (4.9 +/- 0.1 vs. 4.4 +/- 0.1 mmol/l, respectively, P < 0.001) and remained higher at each of the subsequent determinations during the oral glucose tolerance test, although none had a result indicative of either diabetes or impaired glucose tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)

Activity Cycles↗
PubMed1995

Long-term normalization of GLUT 4 protein content in skeletal muscle of streptozotocin-diabetic Lewis rats after islet transplantation.

Islet transplantation under the kidney capsule of STZ-diabetic Lewis rats was able to maintain near-normoglycemia over a period of 6 months. Fasting insulin in these animals was higher compared to controls but did not increase after feeding. Plasma glucose following an OGTT at 2 months was only slightly impaired, and after 6 months was more severely impaired in the Tx rats. An IVGTT 6 months after Tx confirmed impaired glucose tolerance and showed a loss of first phase insulin release. GLUT 4 protein content in skeletal muscle was completely restored in Tx animals. In conclusion, long-term near-normoglycemia after syngeneic islet transplantation under the kidney capsule of STZ-diabetic Lewis rats is associated with complete normalization of skeletal muscle GLUT 4 protein content, even in the presence of abnormal glucose tolerance and impaired insulin secretion.

Animals↗