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Results for “Glucose Intolerance”

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PubMed2001

Gene therapy attenuates the elevated blood pressure and glucose intolerance in an insulin-resistant model of hypertension.

OBJECTIVE: Fructose feeding in male Sprague-Dawley (SD) rats results in a mild hypertension and glucose intolerance. Although the mechanism of this glucose intolerance and hypertension is not completely understood, a role for the renin-angiotensin system (RAS) has been proposed. In the current study our aim was to test the hypothesis that intervention of the RAS with a gene therapy approach would be effective in preventing the development of hypertension and glucose intolerance in this animal model. DESIGN AND METHODS: Five-day-old SD rats were administered either an empty retroviral vector (LNSV) or retroviral vector containing AT1 receptor antisense DNA (AT1R-AS). The virus (25 microl, 8 x 10(9) CFU/ml) was injected into the heart and the animals were returned to their mothers. After weaning, half the animals from each group were placed on breeder's chow or a 60% fructose diet. Indirect blood pressures (BP) were determined and an oral glucose tolerance test (OGTT) was performed when the animals had been on the respective diets for 2 months. RESULTS: Fructose-fed animals developed mild hypertension (145 +/- 3 versus 132 +/- 4 mmHg) by 6 weeks of dietary intervention. This increase in BP was prevented by AT1R-AS treatment (125 +/- 3 mmHg). At 2 months of age, fasting blood glucose was comparable among the four groups; however, the glucose excursion during the OGTT was significantly greater and more prolonged in the LNSV-treated, fructose-fed group than the other three groups. AT1R-AS treatment significantly prevented glucose intolerance in the fructose rat to levels observed in the controls. CONCLUSIONS: Early fructose dietary treatment results in moderate hypertension and glucose intolerance, which is prevented by a single neonatal treatment with AT1R-AS. These results suggest that the RAS is involved in the glucose intolerance associated with fructose feeding and that genetic intervention is effective in this rat model.

Animals↗

PubMed1994

Increased risk factors for coronary artery disease in Japanese subjects with hyperinsulinemia or glucose intolerance.

OBJECTIVE: To understand the interrelationship of coronary artery disease (CAD) risk factors including hyperlipidemia, hypertension, and glucose intolerance to prevent and better manage this disease. RESEARCH DESIGN AND METHODS: We performed a 100-g oral glucose tolerance test in 2,113 subjects, and we evaluated their plasma lipid levels, blood pressure (BP), and plasma glucose and plasma insulin responses. RESULTS: Multiple regression analysis demonstrated a significant relationship of either BP, plasma triglyceride (TG), or high-density lipoprotein (HDL) cholesterol levels to plasma insulin and glucose response after the glucose load. Plasma cholesterol levels were related only to the plasma glucose response. In subjects matched for age, sex, and body mass index (BMI) with hyperinsulinemia or normoinsulinemia, the hyperinsulinemic subjects had a significantly higher mean BP and plasma TG level than the normoinsulinemic subjects (128.8/82.3 vs. 122.9/79.3 mmHg and 172.1 vs. 119.4 mg/dl), and the HDL-cholesterol level was significantly lower (43.9 vs. 47.8 mg/dl). Furthermore, subjects matched for age, sex, and BMI with glucose intolerance had a higher mean BP (128.4/81.8 vs. 123.5/78.7 mmHg) and higher plasma TG level (154.2 vs. 123.0 mg/dl) than those without glucose intolerance. CONCLUSIONS: Based on these findings, subjects with hyperinsulinemia or glucose intolerance should be carefully managed to prevent CAD, because they have more numerous and more severe risk factors than subjects with normal plasma insulin levels or subjects without glucose intolerance.

Blood Glucose↗

PubMed2003

Splanchnic tissues play a crucial role in uremic glucose intolerance.

OBJECTIVE: Determine the mechanism of glucose intolerance in chronically uremic subjects. DESIGN: Comparison of doubly labeled oral glucose tolerance tests. SUBJECTS: Seven nondialyzed chronically uremic subjects (creatinine, 420 +/- 104 micromol/L) and 7 healthy subjects, matched for age and body mass index. INTERVENTION: Plasma glucose was labeled by an infusion of dideuterated glucose started 120 minutes before ingestion of 1 g/kg of naturally 13C-enriched corn starch glucose. Glucose levels and oxidation were monitored for 330 minutes after glucose ingestion. RESULTS: Uremic subjects had normal fasting plasma glucose levels and impaired glucose tolerance with high plasma insulin (P <.001 versus controls). Glucose tolerance was impaired because of an increased total rate of appearance of glucose (cumulated on 330 minutes: uremic, 1,231 +/- 42 mg/kg/330 min, controls, 1,031 +/- 64; P <.05). Peripheral glucose uptake was increased (P <.05) because of an increased nonoxidative disposal (P =.051). CONCLUSIONS: Although peripheral glucose uptake resisted the stimulatory effect of the high insulin levels, glucose tolerance was impaired through splanchnic metabolic disturbances: reduced splanchnic glucose uptake and increased endogenous glucose production. The respective contribution of these abnormalities remains to be determined.

Blood Glucose↗

PubMed2003

Effect of hypertension and hypertension-glucose intolerance on myocardial ischemic injury.

Systemic hypertension and type 2 diabetes mellitus are major risk factors for myocardial infarction. Yet, glucose intolerance, a prelude stage to type 2 diabetes, is associated with reduced infarct size. Since chronic hypertension adversely affects the myocardium, we tested the hypothesis that the coexistence of systemic hypertension and glucose intolerance reverses the cardioprotection associated with impaired glucose tolerance. Hearts from 9-month-old animals were subjected to a 40-minute occlusion of the left coronary artery followed by 2 hours of reperfusion. Before ischemia, similar values for the four experimental groups were observed for the coronary flow, heart rate, and maximum ventricular pressure. During the course of the ischemia-reperfusion insult, the two hypertensive groups displayed greater reductions in contractility than their normotensive counterparts. Infarct size was lower in the normotensive glucose-intolerant rat than in the normotensive control rat. Surprisingly, the hypertrophied hearts of the hypertensive and hypertensive glucose-intolerant rats displayed reduced infarct size (P<0.05). However, raising the afterload pressure from 100 to 160 cm H2O increased infarct size in the two hypertensive groups. This narrowed the differential between the hypertensive glucose-intolerant (160 cm H2O) and the normotensive control (100 cm H2O) rats. Nonetheless, at the higher afterload pressure, infarct size was less in the hypertensive glucose-intolerant rats than in their hypertensive counterparts. In conclusion, the impairment in contractile function despite the reduction in infarct size underscores the increased susceptibility of the hypertrophied, hypertensive heart to ischemic injury. Furthermore, exacerbation of cell death at elevated afterload pressure indicates the potential benefit of aggressive antihypertensive therapy.

Animals↗

PubMed1980

Glucose intolerance due to insulin resistance in patients with spinal cord injuries.

Glucose intolerance occurs frequently in patients with spinal cord injury (SCI). To characterize this better, 45 patients with spinal cord injuries received oral glucose tolerance tests (OGTT). The subjects with glucose intolerance had significantly higher insulin levels than either the glucose-tolerant or normal control subjects. Since hyperinsulinism in the presence of glucose intolerance suggests insulin resistance, the peripheral insulin activity (A) was calculated from the OGTT data. The glucose-intolerant SCI patients had significantly lower A values than the other groups. The most resistant SCI subjects (A < 0.3) also had resistance to exogenous insulin. In 18 subjects receiving insulin tolerance tests, the A value calculated from the OGTT was 100% accurate in predicting the presence of sensitivity or resistance to exogenous insulin. In spite of the presence of insulin resistance, however, 125I-insulin binding to SCI patients' circulating monocytes was not significantly different from that in control subjects.

Blood Glucose↗

PubMed2000

The role of obesity in the association of cardiovascular risk factors and glucose intolerance in small Japanese and North American communities.

To investigate whether the influence of obesity on cardiovascular risk factors and glucose intolerance differs between Japan and the US, we conducted cross-sectional surveys in those with elevated plasma glucose in Tanushimaru, Japan, and a stratified random population sample, in Wadena, MN. Subjects numbered 204 in Tanushimaru and 334 in Wadena. Body mass index (BMI), blood pressure, blood lipids, fasting plasma levels of glucose, glycosylated hemoglobin A(1c,) insulin, and free fatty acids were assessed. Overweight was defined as BMI of 27.5-29.9 kg/m(2) and obesity as BMI> or =30 kg/m(2). Gradual increases in risk factors were seen as BMI increased in both studies. Most risk factors were associated with glucose intolerance, except for BMI in Tanushimaru. In Wadena, glucose intolerance increased sharply among the obese. Adjustment for BMI attenuated the associations of cardiovascular risk factors with glucose intolerance in Wadena, but not in Tanushimaru. Obesity has an exaggerated influence on risk factors, compared with being overweight. The associations of glucose intolerance with cardiovascular risk factors are more affected by adjustment for BMI in Wadena than in Tanushimaru, not because of a different influence of body weight on risk factors between the two cities, but because obesity is rare in Japan.

Adult↗

PubMed2001

Risk factors for glucose intolerance in active acromegaly.

In the present retrospective study we determined the frequency of glucose intolerance in active untreated acromegaly, and searched for risk factors possibly supporting the emergence of the diabetic condition. Among 43 patients, 8 (19%; 95% CI: 8-33%) had diabetes mellitus and 2 (5%; 1-16%) impaired glucose tolerance. No impaired fasting glycemia was demonstrable. The frequency of diabetes was on average 4.5 times higher than in the general Slovak population. Ten factors suspected to support progression to glucose intolerance were studied by comparing the frequency of glucose intolerance between patients with present and absent risk factors. A family history of diabetes and arterial hypertension proved to have a significant promoting effect (P<0.05, chi-square test). A significant association with female gender was demonstrated only after pooling our data with literature data. Concomitant prolactin hypersecretion had a nonsignificant promoting effect. In conclusion, the association of active untreated acromegaly with each of the three categories of glucose intolerance (including impaired fasting glycemia, not yet studied in this connection) was defined as a confidence interval, thus permitting a sound comparison with the findings of future studies. Besides a family history of diabetes, female gender and arterial hypertension were defined as additional, not yet described risk factors.

Acromegaly↗

PubMed1998

Chromium, glucose intolerance and diabetes.

Within the last 5 years chromium (Cr) has been shown to play a role in glucose intolerance, Type 2 diabetes mellitus (Type 2 DM), and gestational diabetes. In addition, diabetes and the neuropathy of a patient on home parenteral nutrition were alleviated when supplemental Cr was added to total parenteral nutrition (TPN) solutions. In a study conducted in China that has been supported by studies in the United States, supplemental Cr as Cr picolinate improved the blood glucose, insulin, cholesterol, and hemoglobin A1C in people with Type 2 DM in a dose dependent manner. Follow-up studies of > 1 year have confirmed these studies. The requirement for Cr is related to the degree of glucose intolerance: 200 microg/day of supplemental Cr is adequate to improve glucose variables of those who are mildly glucose intolerant. However, people with more overt impairments in glucose tolerance and diabetes usually require more than 200 microg/day. Daily intake of 8 microg of Cr per kg body weight was also more effective than 4 microg/kg in women with gestational diabetes. The mechanism of action of Cr involves increased insulin binding, increased insulin receptor number, and increased insulin receptor phosphorylation. In summary, supplemental Cr has been shown to have beneficial effects without any documented side effects on people with varying degrees of glucose intolerance ranging from mild glucose intolerance to overt Type 2 DM.

Chromium↗

PubMed1988

Clinically significant diuretic-induced glucose intolerance.

Diuretic-induced glucose intolerance is cited frequently as a problem of only limited clinical significance. In certain populations, such as Mexican-Americans, this effect may be much more dramatic. A 50-year-old obese Mexican-American woman presented with a three-month history of increased thirst and frequent urination. A fasting blood glucose concentration of 365 mg/dL prompted initiation of chlorpropamide therapy. A review of her medical history revealed that a thiazide diuretic was started six months previously. A reduction in thiazide dose and potassium supplementation together with chlorpropamide therapy controlled the patient's blood glucose. Subsequently, all three medications were discontinued, and the patient remained normoglycemic during a full year of follow-up. The temporal relationship between symptomatic diabetes and hydrochlorothiazide therapy incriminates the diuretic as the most probable cause.

Benzothiadiazines↗

PubMed1993

Detection of glucose intolerance in pregnancy.

Current methods for the screening and diagnosis of glucose intolerance first discovered in pregnancy are reviewed and innovative approaches to the detection of metabolic disturbances in pregnancy are presented. Glucose intolerance first detected in pregnancy, termed gestational diabetes mellitus (GDM), is amongst the most significant risks of adverse fetal and maternal outcome. Normal pregnancy is characterized by both insulin resistance and pancreatic B cell compensation. In those pregnancies complicated by glucose intolerance reflected in hyperglycemia, insulin resistance appears to be heightened, both blood flow and transcapillary transport of insulin are compromised and insulin receptor and post receptor defects are exacerbated. The resulting hyperinsulinemia and hyperglycemia have, in turn, been associated with accumulated maternal fat deposition and fetal macrosomia. This cascade of events constitutes GDM or impaired glucose tolerance. The discovery of GDM is made through a process of screening and diagnosis, employing standardized oral glucose challenge tests. These tests were designed to identify those women at risk for subsequent development of non-insulin dependent diabetes mellitus. The current efficacy of glucose challenge tests has been questioned in light of increasing concern over their usefulness in detecting those women at risk for maternal and fetal complications of pregnancy. Alternative methods, including both the modification of the standardized tests, as well as the introduction of newer methodologies, such as capillary blood glucose monitoring, have been proposed. The implementation of newer approaches may result in improved detection of those women whose infants are at high risk for both metabolic and morphologic complications of persistent hyperglycemia in pregnancy.

Diabetes, Gestational↗

PubMed1985

[Clinical study on glucose intolerance and insulin response in obstructive jaundice].

Insulin responses to oral glucose loads were studied in patients with obstructive jaundice and compared with those of other liver diseases (fatty liver, chronic hepatitis and liver cirrhosis), pancreatic diseases, and definite diabetes mellitus. Compared with their corresponding glucose intolerance, high insulin responses were characteristic in fatty liver, chronic hepatitis and liver cirrhosis, and insulin responses and insulinogenic index decreased in chronic hepatitis and liver cirrhosis as glucose intolerance progressed. In obstructive jaundice with the pancreatic ducts stenotic or obstructed, insulin responses were suppressed in comparison with their corresponding glucose intolerance, and also insulinogenic index were below 0.5 in most of the cases. However, in obstructive jaundice with the pancreatic ducts intact, high insulin responses were observed in almost half of the cases with insulinogenic index above 0.5, and insulin response and insulinogenic index decreased as glucose intolerance progressed. While most cases of fatty liver, chronic hepatitis and liver cirrhosis with insulinogenic index above 0.5 were distributed in non-diabetes zone in sigma BS-sigma IRI plane (Kosaka's), those with insulinogenic index below 0.5 were distributed in intermediate zone. Most cases with obstructive jaundice with pancreatic ducts stenotic or obstructed, had insulinogenic index below 0.5 and were distributed in diabetes zone. However, half of cases with obstructive jaundice with pancreatic ducts intact, had insulinogenic index above 0.5 and their distribution in non-diabetes zone, while the other half had insulinogenic index below 0.5 and their distribution in diabetes zone. Therefore, it may be concluded that insulin responses increase at the early stage of obstructive jaundice mainly under influence of liver dysfunction itself, but that insulin response is suppressed at later stage of obstructive jaundice as pancreatic islets are affected.

Blood Glucose↗

PubMed1980

Classification of glucose intolerance in the aged based on hemoglobin A1.

While the incidence of glucose intolerance increases with age, the diagnostic criteria of diabetes mellitus in the aged have been controversial. In this study, glucose intolerance in the aged was classified according to the changes in Hb A1 concentrations and plasma glucose levels at the time of 50 g oral glucose tolerance test. Ninety-six aged Japanese (60-90 years old, mean 72 years) were studied. Hb A1 was measured by Fast Hb Test System. The results suggested the existence of critical plasma glucose levels for the increment in Hb A1 in the aged, and the critical values were around 120 mg/100 ml at fasting, and around 240 mg/100 ml at 60 or 120 min after glucose load. Using these critical plasma glucose levels, glucose intolerance in the aged was classified into two groups, i.e., Group 1 with fasting plasma glucose below 120 mg/100 ml and both plasma glucose levels at 60 and 120 min below 240 mg/100 ml, and Group 2 with fasting plasma glucose above 120 mg/100 ml and both plasma glucose levels at 60 and 120 min above 240 mg/100 ml. The incidence of elevated Hb A1 in Group 1, 4.3%, was significantly lower than 94.1% in Group 2, and insulinogenic index at 30 min in Group 1, 0.74, was significantly higher than 0.07 in Group 2. In conclusion, it was proposed that subjects in Group 2 represent diabetes mellitus, while subjects in Group 1 might not be of pathological glucose intolerance in the aged.

Aged↗

PubMed2001

Diabetes Screening in Canada (DIASCAN) Study: prevalence of undiagnosed diabetes and glucose intolerance in family physician offices.

OBJECTIVE: To assess the prevalence of undiagnosed diabetes and glucose intolerance in individuals > or =40 years of age who contacted their family physician for routine care. RESEARCH DESIGN AND METHODS: The study used a stratified randomized selection of family physicians across Canada that was proportional to provincial and urban/rural populations based on Statistics Canada Census data (1996). Consecutive patients > or =40 years of age were screened for diabetes. If a casual fingerprick blood glucose was >5.5 mmol/l, the patient returned for a fasting venous blood glucose test. If the fasting blood glucose was 6.1-6.9 mmol/l, a 2-h 75-g post-glucose load venous blood glucose was obtained. Results of these tests were used to classify patients in diagnostic categories. RESULTS: Data were available for 9,042 patients. Previously undiagnosed diabetes was discovered in 2.2% of the patients, and new glucose intolerance was found in an additional 3.5% of patients. Overall, 16.4% of patients had previously known diabetes. The decrease in fasting plasma glucose criterion from 7.8 to 7.0 mmol/l resulted in a 2.2% versus a 1.6% prevalence of new diabetes. Several risk factors were reported in a significantly greater proportion of patients with new glucose intolerance and either new and known diabetes compared with the normal glucose tolerance group of patients. CONCLUSIONS: Routine screening for diabetes by family physicians is justified in patients > or =40 years of age, given the finding of previously undiagnosed diabetes in 2.2% of these patients and newly diagnosed glucose intolerance in an additional 3.5% of these patients. Another 16.4% of primary care patients > or =40 years of age have known diabetes. This has important implications regarding health resources and physician education.

Adult↗

PubMed1994

Glucose intolerance in liver cirrhosis: role of hepatic and non-hepatic influences.

Oral glucose tolerance was tested in a heterogeneous group of 108 patients with liver cirrhosis. Data were compared with those from 181 subjects without liver disease (44% normal, 35% impaired glucose tolerance and 21% type 2 diabetes mellitus). In cirrhosis, 27% of the patients had normal, 36% had impaired glucose tolerance, and 37% were diabetic. There was no association between glucose intolerance or diabetes and the aetiology of cirrhosis, the duration of the disease, the biochemical indicators of hepatocyte damage, cholestasis and/or liver function. Only weak associations were found between the results of quantitative liver functions tests (caffeine, xylocaine, indocyanine green) and basal and post load glucose and insulin concentrations. Cirrhotics with 1st degree relatives with type 2 diabetes mellitus (n = 16) did not show an increased prevalence of diabetes. Older and/or malnourished patients were more frequently glucose intolerant. Using the plasma glucose concentration 120 minutes after glucose load as the dependent variable, multivariate regression analysis showed that 54% of its variance is associated with the following variables: basal plasma glucose (36%) and free fatty acid concentration (5%), age (3%), basal glucose oxidation rate (3%), muscle mass (3%) and plasma free glycerol at 120 minutes after glucose load (3%). By contrast, the clinical state of the patients (i.e. the CHILD-Pugh score) accounted for only 2% of the variance. We conclude that glucose tolerance is variable in cirrhosis. After manifestation of liver disease, glucose intolerance or diabetes cannot be explained by the clinical, histological or biochemical signs of liver disease.

Adult↗

PubMed2002

Distinct role of adiposity and insulin resistance in glucose intolerance: studies in ventromedial hypothalamic-lesioned obese rats.

It remains unclear whether adiposity plays an important role in glucose intolerance independently of insulin resistance. We investigated whether adiposity and insulin resistance had distinct roles in glucose intolerance in rats. We examined glucose tolerance and insulin resistance using ventromedial hypothalamic (VMH)-lesioned rats in the dynamic and the static phases of obesity (2 and 14 weeks after lesioning, respectively). Rats were fed either normal chow or a fructose-enriched diet (60% of total calories). The intravenous glucose tolerance test (IVGTT) was performed by bolus injection of glucose solution (1 g/kg) and blood sampling after 0, 5 10, 30, and 60 minutes. Insulin resistance was evaluated from the steady-state plasma glucose (SSPG) value during continuous infusion of glucose, insulin, and somatostatin. SSPG was not increased in VMH-lesioned rats in the dynamic phase of obesity, but increased markedly in the static phase. The area under the glucose curve (glucose AUC) during IVGTT was increased in VMH-lesioned rats in the static phase, but not in the dynamic phase, when compared with their sham-operated counterparts. A fructose-enriched diet for 2 or 14 weeks increased SSPG values to a similar extent in both sham-operated and VMH-lesioned rats without inducing excess adiposity, but glucose intolerance was only developed in the obese rats. The plasma leptin level, an excellent indicator of adiposity, was significantly related to the glucose AUC independently of the insulin level. Insulin resistance or increased adiposity alone is not sufficient to impair glucose tolerance, but increased adiposity plays an important role in the development of glucose intolerance in an insulin-resistant state.

Animals↗

PubMed1996

[Glucose intolerance in chronic renal failure].

It has been recognized that glucose intolerance is a common finding in patients with chronic renal failure (CRF). Insulin resistance and impaired insulin secretion contribute to the pathogenesis of glucose intolerance. The resistance to insulin action is commonly observed in chronic renal failure and mainly due to impaired glucose uptake by muscle. In contrast, insulin secretion in response to hyperglycemia is variable: increased, decreased and normal. Recent studies reported that high PTH levels impaired insulin secretion from pancreatic islets. In this review, we mention the mechanism of glucose intolerance in chronic renal failure.

Glucose Intolerance↗

PubMed2005

Stable agonist of glucose-dependent insulinotropic polypeptide (GIP) restores pancreatic beta cell glucose responsiveness but not glucose intolerance in aging mice.

Glucose tolerance progressively declines with age whilst the onset of type two diabetes increases dramatically. Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-induced insulin secretion. The present study was designed to assess the insulinotropic effects of a potent long-acting GIP receptor agonist, N-AcGIP(LysPAL37), in aging mice. In older mice, body weights, basal plasma glucose and insulin concentrations were significantly higher than in young mice (P<0.05 to P<0.001). Intraperitoneal injection of glucose alone (18 mmol/kg body weight) revealed a significantly lower (P<0.05) insulin response in older mice, which was accompanied by impaired glucose tolerance (P<0.05). Normal glucose-mediated insulin secretion was restored in N-AcGIP(LysPAL37) treated older mice. However the glycaemic excursion remained significantly impaired in older mice (P<0.05), suggestive of impaired insulin action. Native GIP had a similar overall effect in younger and older mice. These data indicate that N-AcGIP(LysPAL37) is able to counter the age-related deterioration of pancreatic beta cell glucose sensitivity and insulin secretion.

Aging↗

PubMed1985

Pathogenesis of age-related glucose intolerance in man: insulin resistance and decreased beta-cell function.

To identify the pathogenic factors responsible for glucose intolerance of aging, we measured a variety of metabolic parameters, including insulin sensitivity and islet cell function, in 10 young (18-36 yr old) and 10 older (57-82 yr old) men of normal body weight. Subject groups had equivalent fasting plasma glucose and fat cell size values. Frequently sampled iv glucose tolerance tests were performed, and the data were analyzed by computer using the minimal model approach. This technique yields the following measures: SI, the insulin sensitivity index; phi 1 and phi 2, indices of first and second phase beta-cell responsiveness to glucose; n, fractional insulin clearance, and SG, a measure of dynamic glucose disappearance dependent on glucose per se. We also evaluated beta-cell responsiveness independently by measuring the plasma insulin response to arginine injections at three levels of glycemia and calculated potentiation slope from the relationship between the acute insulin response to arginine and the prestimulus glucose level. The older men were glucose intolerant (glucose disappearance rate, 1.32% min-1) compared to the younger men (glucose disappearance rate, 2.21% min-1; P less than 0.01). This intolerance was the result of both a beta-cell defect and insulin resistance. The potentiation slope (r = -0.67; P less than 0.02) and phi 2 (r = -0.47; P less than 0.05) both decreased with age. In addition, SI in the older group was diminished 63% (2.4 vs. 6.5; 10(-4) min-1/microU/ml; P less than 0.001) and was unrelated to differences in body fat. No differences were found in either n or SG. These studies suggest that the diminished glucose tolerance of aging in normal weight men has multifactorial causality. Both beta-cell dysfunction and insulin resistance are important. In contrast, we found little evidence for changes in insulin clearance or insulin-independent glucose disappearance contributing to age-related glucose intolerance.

Adipose Tissue↗