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Biomedical subjects

E Ferrannini

Publications and source records attributed to E Ferrannini.

At least 127 records · Page 7Linked to original sources
PubMed1995

Physiological and metabolic consequences of obesity.

Fasting plasma insulin levels provide an indirect indication of insulin resistance. Glucose utilization rate, measured by the euglycemic clamp technique, is a direct measure of insulin sensitivity. Insulin sensitivity decreases with increasing body mass index (BMI) in the range of 27 to 35 kg/m2. A higher waist-to-hip ratio is associated with lower insulin sensitivity, after adjusting for BMI. Obese patients have higher plasma free fatty acid levels and less suppression of lipolysis by insulin than lean individuals. The increased supply of fatty substrates and their competition with glucose for oxidation constitute a component of insulin resistance in obesity. Both systolic and diastolic blood pressure are increased with BMI. The hemodynamic effects may be due to an increase in cardiac output and enhanced activity of the adrenergic nervous system.

Blood Pressure↗
PubMed1995

Effect of insulin on uric acid excretion in humans.

Although hyperuricemia is a frequent finding in insulin-resistant states, insulin's effect on renal uric acid (UA) handling is not known. In 20 healthy volunteers, diastolic blood pressure, body weight, and fasting plasma insulin were positively (and age was negatively) related to fasting plasma UA concentrations, together accounting for 53% of their variability. During an insulin clamp, urine flow was lower than during fasting conditions (1.01 +/- 0.12 vs. 1.56 +/- 0.32 ml/min, P = 0.04), whereas creatinine clearance was unchanged (129 +/- 7 and 131 +/- 9 ml/min, P = not significant). Hyperinsulinemia did not alter serum UA concentrations (303 +/- 13 vs. 304 +/- 12 microM) but caused a significant decrease in urinary UA excretion [whether expressed as absolute excretion rate (1.66 +/- 0.21 vs. 2.12 +/- 0.23 mumol/min, P = 0.03), clearance rate (5.6 +/- 0.8 vs. 7.3 +/- 0.8 ml/min, P = 0.03), or fractional excretion (4.48 +/- 0.80 ml/min vs. 6.06 +/- 0.64%, P < 0.03)]. Hyperinsulinemia was also associated with a 30% (P < 0.001) fall in urine Na excretion. Fractional UA excretion was related to Na fractional excretion under basal conditions (r = 0.59, P < 0.01) and during the insulin period (r = 0.53, P < 0.02). Furthermore, the insulin-induced changes in fractional UA and Na excretion correlated with one another (r = 0.66, P < 0.001). Physiological hyperinsulinemia acutely reduces urinary UA and Na excretion in a coupled fashion.

Adult↗
PubMed1995

Insulin resistance in microalbuminuric hypertension. Sites and mechanisms.

Microalbuminuria in patients with essential hypertension is a marker of incipient glomerular dysfunction and clusters with lipid and hemodynamic abnormalities. Recent evidence has shown that hypertensive patients with microalbuminuria have a hyperinsulinemic response to oral glucose, suggesting the presence of insulin resistance. To directly test this possibility we studied insulin action in two accurately matched groups (n = 10 each) of hypertensive patients with or without microalbuminuria (14 +/- 2 versus 52 +/- 7 mg/24 h-1, mean of three 24-hour collections). In response to glucose ingestion microalbuminuric patients showed slight hyperglycemia (area under the curve, 928 +/- 43 versus 784 +/-19 nmol/L-1/2h-1, P < .02) and a marked hyperinsulinemia (26.8 +/- 3.3 versus 49.8 +/- 3.7 nmol/L-1/2h-1, P < 0.01). Basal arterial blood pressure, heart rate, and forearm blood flow were similar in the two groups and did not change significantly during a 2-hour euglycemic insulin clamp. Insulin-stimulated wholebody glucose uptake was 25% lower in microalbuminuric patients (33.5 +/- 2.5 versus 25.2 +/- 2.1 mumol/min-1/kg-1, P < .02). This difference was entirely due to a 40% reduction in glycogen synthesis (12.9 +/- 1.8 versus 21.3 +/- 3.2 mumol/min-1/kg-1, P < .05) as glucose oxidation was similarly stimulated in the two groups. In contrast there was no difference in the ability of insulin to suppress hepatic glucose production (by approximately 100% at the end of the clamp), to decrease fractional sodium and potassium excretions (by 35%), to lower circulating free fatty acids (by 80%), and to reduce plasma potassium concentrations (by 10%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Kinetic analysis of thyroid hormone action on glucose metabolism in man.

Thyroid hormone action on insulin's effect on glucose kinetics was investigated with the use of a physiological three compartment model. In six healthy volunteers before and after 14 days of thyroxine treatment (300 micrograms/day), a bolus of [3-H3]glucose was injected and the time course of plasma radioactivity was followed closely for 150 min. Then a hyperinsulinemic (1 mU.min-1.kg-1) and euglycemic clamp was started, and euglycemia was maintained for another 250 min. A second bolus of the tracer was then given at 240 min, and the plasma radioactivity was followed for 160 min. Insulin stimulated basal plasma glucose clearance fourfold (p < 0.001) and completely suppressed basal hepatic glucose production (p < 0.001). Concomitantly, the total distribution volume of glucose was increased by 19% (p < 0.05); this change was accompanied by about 50% expansion of the slowly exchanging glucose pool (putatively representing the insulin-dependent compartment). Thyroxine treatment increased plasma triiodothyronine by about 20% (0.1 > p > 0.05) but did not affect basal glucose turnover, insulin-stimulated plasma glucose clearance or the insulin-induced suppression of endogenous glucose output. However, thyroxine treatment blunted the insulin-induced increases in total distribution volume and the slowly exchanging pool of glucose (p = NS vs the basal state). We conclude that minor changes in plasma triiodothyronine (such as occur during overfeeding) do not interfere with the ability of insulin to stimulate the rate of disappearance of glucose or suppress endogenous glucose release; however, our data suggest that they induce finer changes in glucose kinetics, possibly reflecting acceleration or intracellular glucose degradation.

Adult↗
PubMed1995

Potential risk of myopathy by HMG-CoA reductase inhibitors: a comparison of pravastatin and simvastatin effects on membrane electrical properties of rat skeletal muscle fibers.

To get insight into the potential risk of myopathy associated with therapy involving 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, we evaluated in vivo and in vitro the effects of a daily 2 to 3-month treatment with pravastatin (100 mg/kg) and with simvastatin (5, 10 and 50 mg/kg) on the electrical properties of rat skeletal muscle fibers. The electromyographic activity revealed no sign of myopathy during treatment with pravastatin and with simvastatin. At the end of the treatment, the passive and active membrane electrical parameters of the extensor digitorum longus muscles were measured in vitro by computerized two-intracellular-microelectrode technique. A dose-dependent reduction of membrane chloride conductance was recorded in extensor digitorum longus fibers of simvastatin-treated groups, and at 50 mg/kg the reduction of chloride conductance was significant in 6 out of the 7 treated rats. By contrast, none of the pravastatin-treated rats showed significant alteration of chloride conductance. Consequently, the excitability parameters were modified by simvastatin but not by pravastatin treatment, whereas the resting membrane potential was not affected. An increase in potassium conductance, reduced by in vitro application of glybenclamide, was recorded in 30% of the simvastatin-treated rats (50 mg/kg) and in only 15% of the pravastatin-treated rats. Our results suggest that the risk of myopathy is much higher with the lipophilic simvastatin than with the hydrophilic pravastatin and support the hypothesis that the muscle toxicity of HMG-CoA reductase inhibitors is due to an intracellular action mediated by the inhibition of muscle cholesterol synthesis.

Animals↗
PubMed1994

Glucose absorption and production following oral glucose: comparison of compartmental and arteriovenous-difference methods.

Both whole-body models and the regional arteriovenous (AV)-difference method have been used to calculate systemic glucose rates of appearance (Ras) under non-steady-state conditions. Although whole-body models have been experimentally validated in the dog, direct comparison of the whole-body and regional-balance approach has not been made in man. We reanalyzed published data obtained by combining the double-tracer technique ([3H]glucose infusion with ingestion of a [14C]glucose-labeled load) with hepatic vein catheterization. Steele's monocompartmental model underestimated the Ra of oral glucose ([RaO] by 12%, P < .0001) and overestimated the Ra of endogenous glucose ([RaE] by 19%, P < .0001) in comparison to a two-compartment (2-c) model calculation. Splanchnic balance data were used to compute the total glucose Ra (RaT) with either steady-state or non-steady-state equations (the latter by estimating splanchnic transit times). Except for one early time point (15 minutes), the two calculations agreed well with one another. The glucose RaT by the balance method was well correlated with that calculated by the 2-c whole-body model (r = .72, P < .0001 on all data points); however, the former significantly underestimated the latter by 0.62 mg.min-1.kg-1 (or 13%, P < .01) on average throughout the absorptive period. This bias was small in comparison to the estimated random error affecting the calculation of glucose RaT by the model, which averaged 1.4 mg.min-1.kg-1 (corresponding to a variation coefficient of approximately 30%).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1994

Glycogen turnover during refeeding in the postabsorptive dog: implications for the estimation of glycogen formation using tracer methods.

Recent 13C nuclear magnetic resonance (13C-NMR) studies in the anesthetized rat and perfused liver suggest that hepatic glycogen is simultaneously synthesized and degraded, even during combined hyperglycemia and hyperinsulinemia. The presence of glycogen turnover would confound efforts to study glycogen repletion with the use of tracer methods during feeding, particularly if the liver is not glycogen-depleted. To ascertain whether glycogen turnover occurs during normal feeding, we measured liver uptake of glucose in 10 awake, healthy, postabsorptive dogs with long-term arterial, portal, and hepatic venous catheters before and for 3 hours after a meal of either glucose alone (1.5 g/kg) or glucose supplemented with crystalline amino acids (0.7 g/kg); the meal was labeled with D-[3-3H]glucose and [U-14C]alanine. Liver glycogen level was measured in biopsies obtained before and at 180 minutes after the meal. The postabsorptive liver glycogen content was 4.3 +/- 0.9 g/100 g, and net hepatic glucose release averaged 1.8 +/- 0.3 mg/min/kg. Over the 3 hours following feeding, the liver took up glucose (0.37 +/- 0.14 and 0.33 +/- 0.16 g/kg body weight in dogs receiving glucose and glucose with amino acids, respectively). At 3 hours, glycogen synthesis from D-[3-3H]glucose in the two groups averaged 0.24 +/- 0.09 and 0.22 +/- 0.05 g/kg, or approximately 15% of the ingested glucose load. 14C-glucose also was found in liver glycogen, demonstrating ongoing hepatic gluconeogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1994

Insulin resistance and hypertension: studies in transgenic hypertensive TGR(mREN-2)27 rats.

The link between hyperinsulinemia and hypertension is imperfectly understood. Recently, a renin gene (the mouse DBA/REN-2d gene) has been transfected into rats, leading to high blood pressure in transgene-positive animals, TGR(mREN-2)27 rats. We tested whether heterozygous hypertensive TGR(mREN-2)27 rats presented evidence of insulin resistance in comparison with the parent strain of Sprague-Dawley rats. Despite their higher blood pressure (203 +/- 8 vs. 112 +/- 6 mmHg, P < 0.001), transgenic rats had normal fasting levels of plasma glucose, insulin, free fatty acids, and triglycerides and had normal fasting rates of hepatic glucose production (by [14C]glucose infusion). During a euglycemic hyperinsulinemic clamp (3 mU/min), stimulation of whole body glucose utilization was equivalent in transgenic and control animals (12.6 +/- 0.6 vs. 10.9 +/- 1.0 mg.min-1.kg-1, respectively). Likewise, suppression of hepatic glucose output by insulin was complete in both groups. The glucose utilization index (as measured by the 2-deoxy-D-[3H]glucose technique) was similar between transgenic and control animals in several skeletal muscles (soleus, extensor digitorum longus, tibialis, diaphragm, white and red quadriceps, and white and red gastrocnemius), in white adipose tissue (periovarian and inguinal), and in brown adipose tissue. We conclude that single gene hypertension does not alter whole body and individual tissue insulin sensitivity.

Adipose Tissue↗
PubMed1994

Elevated serum insulin levels in patients with essential hypertension and microalbuminuria.

Hyperinsulinemia, insulin resistance, or both have been described in patients with essential hypertension. Previous work from our laboratory has shown that in hypertensive patients with microalbuminuria, dyslipidemia and abnormal patterns in the diurnal variations of blood pressure are frequently associated. Whether hyperinsulinemia and microalbuminuria are directly related has not been determined. To test this possibility, we measured the plasma insulin response to an oral glucose load in 25 patients with or without microalbuminuria and 20 normotensive control subjects. Serum lipid profile and 24-hour ambulatory blood pressure were obtained. In the hypertensive patients as a group, the plasma insulin response to glucose (evaluated as the insulin area under the curve) was significantly enhanced compared with a group of 20 normotensive healthy control subjects (46,311 +/- 3745 and 27,557 +/- 2563 pmol/L x 2 hours, P < .01). When the hypertensive patients were subdivided according to their albumin excretion rate, the microalbuminuric patients had significantly higher plasma glucose (969 +/- 45.2 versus 762 +/- 28.7 mmol/L x 2 hours, P < .01) and insulin (59,172 +/- 5964 versus 37,737 +/- 3422 pmol/L x 2 hours, P < .01) area under the curve values. In addition, a significant direct correlation was found to exist between insulin area under the curve and the urinary albumin excretion rate (r = .63, P < .001). Serum levels of lipoprotein(a) were significantly greater (P < .01) in patients with than in those without microalbuminuria and in control subjects. Furthermore, daytime diastolic blood pressure and nighttime systolic and diastolic blood pressure values were greater in patients with than in those without microalbuminuria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Insulin resistance and vasodilation in essential hypertension. Studies with adenosine.

Insulin-mediated vasodilation has been proposed as a determinant of in vivo insulin sensitivity. We tested whether sustained vasodilation with adenosine could overcome the muscle insulin resistance present in mildly overweight patients with essential hypertension. Using the forearm technique, we measured the response to a 40-min local intraarterial infusion of adenosine given under fasting conditions (n = 6) or superimposed on a euglycemic insulin clamp (n = 8). In the fasting state, adenosine-induced vasodilation (forearm blood flow from 2.6 +/- 0.6 to 6.0 +/- 1.2 ml min-1dl-1, P < 0.001) was associated with a 45% rise in muscle oxygen consumption (5.9 +/- 1.0 vs 8.6 +/- 1.7 mumol min-1dl-1, P < 0.05), and a doubling of forearm glucose uptake (0.47 +/- 0.15 to 1.01 +/- 0.28 mumol min-1dl-1, P < 0.05). The latter effect remained significant also when expressed as a ratio to concomitant oxygen balance (0.08 +/- 0.03 vs 0.13 +/- 0.04 mumol mumol-1, P < 0.05), whereas for all other metabolites (lactate, pyruvate, FFA, glycerol, citrate, and beta-hydroxybutyrate) this ratio remained unchanged. During euglycemic hyperinsulinemia, whole-body glucose disposal was stimulated (to 19 +/- 3 mumol min-1kg-1), but forearm blood flow did not increase significantly above baseline (2.9 +/- 0.2 vs 3.1 +/- 0.2 ml min-1dl-1, P = NS). Forearm oxygen balance increased (by 30%, P < 0.05) and forearm glucose uptake rose fourfold (from 0.5 to 2.3 mumol min-1dl-1, P < 0.05). Superimposing an adenosine infusion into one forearm resulted in a 100% increase in blood flow (from 2.9 +/- 0.2 to 6.1 +/- 0.9 ml min-1dl-1, P < 0.001); there was, however, no further stimulation of oxygen or glucose uptake compared with the control forearm. During the clamp, the ratio of glucose to oxygen uptake was similar in the control and in the infused forearms (0.27 +/- 0.11 and 0.23 +/- 0.09, respectively), and was not altered by adenosine (0.31 +/- 0.9 and 0.29 +/- 0.10). We conclude that in insulin-re15-76sistant patients with hypertension, adenosine-induced vasodilation recruits oxidative muscle tissues and exerts a modest, direct metabolic effect to promote muscle glucose uptake in the fasting state. Despite these effects, however, adenosine does not overcome muscle insulin resistance.

Adenosine↗
PubMed1994

Acute antihyperglycemic mechanisms of metformin in NIDDM. Evidence for suppression of lipid oxidation and hepatic glucose production.

To establish the antihyperglycemic mechanisms of metformin in non-insulin-dependent diabetes mellitus (NIDDM) independently of the long-term, aspecific effects of removal of glucotoxicity, 21 NIDDM subjects (14 obese, 7 nonobese) were studied on two separate occasions, with an isoglycemic (plasma glucose approximately 9 mM) hyperinsulinemic (two-step insulin infusion, 2 h each, at the rate of 4 and 40 mU.m-2.min-1) clamp combined with [3-3H]glucose infusion and indirect calorimetry, after administration of either metformin (500 mg per os, at -5 and -1 h before the clamp) or placebo. Compared with placebo, hepatic glucose production (HGP) decreased approximately 30% more after metformin (from 469 +/- 50 to 330 +/- 54 mumol/min), but glucose uptake did not increase. Metformin suppressed free fatty acids (FFAs) by approximately 17% (from 0.42 +/- 0.04 to 0.35 +/- 0.04 mM) and lipid oxidation by approximately 25% (from 4.5 +/- 0.4 to 3.4 +/- 0.4 mumol.kg-1.min-1) and increased glucose oxidation by approximately 16% (from 16.2 +/- 1.4 to 19.3 +/- 1.3 mumol.kg-1.min-1) compared with placebo (P < 0.05), but did not affect nonoxidative glucose metabolism, protein oxidation, or total energy expenditure. Suppression of FFA and lipid oxidation after metformin correlated with suppression of HGP (r = 0.70 and r = 0.51, P < 0.001). The effects of metformin in obese and nonobese subjects were no different. We conclude that the specific, antihyperglycemic effects of metformin in the clinical condition of hyperglycemia in NIDDM are primarily due to suppression of HGP, not stimulation of glucose uptake, and are mediated, at least in part, by suppression of FFA and lipid oxidation.

Adult↗
PubMed1994

Insulin and the renin-angiotensin-aldosterone system: influence of ACE inhibition.

This article focuses on the links between insulin and blood pressure at the level of the renin-angiotensin-aldosterone system (RAAS). The effects of insulin on plasma potassium levels and whole-body potassium content and the effect of potassium on glucose-induced insulin release identify a physiological glucose-potassium cycle. The normal interactions of insulin and hyperglycemia with the hormones of the RAAS are reviewed, and their changes in patients with diabetes mellitus are discussed. Some key findings on the interrelationships of insulin and the RAAS with regard to sodium metabolism are also brought into focus. A role for changes in the RAAS secondary to insulin resistance, hyperinsulinemia, and hyperglycemia is delineated in relation to the excess hypertension of diabetes. The effects of angiotensin-converting enzyme inhibition on insulin sensitivity and glucose tolerance are reviewed in the context of the glucose-potassium cycle.

Aging↗
PubMed1994

Effect of chronic ACE inhibition on glucose tolerance and insulin sensitivity in hypertensive type 2 diabetic patients.

We studied 14 moderately overweight Type 2 diabetic patients with essential hypertension in stable metabolic control after a run-in period, and again after 3 months of antihypertensive treatment with the angiotensin-converting enzyme (ACE) inhibitor captopril. Glucose tolerance was tested with a 75g oral glucose load (OGTT) and insulin sensitivity was measured by the insulin suppression test (IST) while dietary and drug treatment of the hyperglycemia was maintained constant. In the whole group, mean blood pressure (MBP) fell progressively over 3 months from a baseline value of 123 +/- 3 mmHg (1 mmHg = 0.133 kpa) to a final value of 115 +/- 2 mmHg (P < 0.005). After treatment, fasting plasma glucose, insulin, free fatty acid (FFA), potassium, and glycosylated hemoglobin concentrations were unchanged from baseline. There were no significant differences in glucose tolerance and insulin sensitivity between pre- and post-treatment values. Neither endogenous (oral glucose) nor exogenous (IST) insulin caused any change in plasma potassium concentration. This resistance to the hypokalemic action of insulin was not affected by captopril.

Blood Glucose↗
PubMed1993

Some metabolic aspects of essential hypertension and its treatment.

We tested whether patients with essential hypertension (EH) have metabolic evidence of increased adrenergic activity, and if a relationship exists between carbohydrate metabolism and the blood pressure (BP) response to angiotensin-converting enzyme (ACE) inhibition. Study 1 included 59 subjects who underwent resting ambulatory BP, heart rate, and resting energy expenditure (REE) measurement (by indirect calorimetry). REE was directly related to lean body mass (LBM) (r = 0.56, p < 0.0001) and to fasting plasma insulin levels (p < 0.03), after adjusting for LBM and age) but not to BP. The 38 subjects with EH had significantly higher fasting plasma insulin levels (54 +/- 4 vs 42 +/- 4 pM; p < 0.05) than the 21 normotensive subjects. When normalized by the LBM, the hypertensive patients had significantly higher REE values than the normotensive subjects (89 +/- 2 vs 78 +/- 3 J min-1.kg-1; p < 0.005). No differences in the other measured variables were found between the two groups. Thus, in this group of lean patients with stable EH, relative hyperinsulinemia is associated with a small increase in REE, the significance of which remains to be determined. In study 2, 20 patients with EH received an oral glucose tolerance test and a euglycemic insulin clamp before and after 3 months of treatment with cilazapril. Glucose-induced insulin response, but not insulin sensitivity, was improved by treatment in the whole group. Before therapy, the 12 responders (diastolic BP < 95 mm Hg) had similar glucose tolerance and insulin sensitivity to the eight nonresponders. Responders, however, had lower fractional potassium excretion than nonresponders both during fasting (9.6 +/- 1 vs 16.0 +/- 2.4%; p < 0.02) and during the glucose load (9.1 +/- 1.4 vs 13.1 +/- 1.1%; p < 0.04). In the responders, fasting potassium levels at baseline were directly related to the decrease in BP (p < 0.01) and to the improvement of glucose-induced insulin response (p < 0.04) achieved after treatment. Thus, the therapeutic effect of ACE inhibition is in part related to fractional potassium excretion, which, in turn, affects glucose tolerance through the influence of potassium levels on glucose-induced insulin release.

Adult↗
PubMed1993

Relation of birthweight to maternal plasma glucose and insulin concentrations during normal pregnancy.

Maternal diabetes mellitus is complicated by fetal macrosomia and predisposes the offspring to diabetes, but recent evidence indicates that a low, not high, birthweight is associated with a higher incidence of Type 2 (non-insulin dependent) diabetes in adult life. To clarify the relationships between maternal glucose and insulin levels and birthweight, we measured oral glucose tolerance and neonatal weight in a large group (n = 529) of women during the 26th week of pregnancy. Women with gestational diabetes (n = 17) had more familial diabetes, higher pre-pregnancy body weight, and tended to have large-for-gestational-age babies. In contrast, women with essential hypertension (n = 10) gave birth to significantly (p < 0.01) smaller babies. In the normal group (without gestational diabetes or hypertension, n = 503), maternal body weight before pregnancy and at term, maternal height, week of delivery, gender of the newborn, and parity were all significant, independent predictors of birthweight, together explaining 23% of the variability of neonatal weight. In addition, both fasting (p < 0.006) and 2-h post-glucose (p = 0.03) maternal plasma glucose concentrations were positively associated with birthweight independent of the other physiological determinants, accounting, however, for only 10% of the explained variability. In a subgroup of 134 normal mothers with pre-pregnancy body mass index of less than 25 kg.m-2, in whom plasma insulin measurements were available, the insulin area-under-curve was inversely related to birthweight (p < 0.02) after simultaneously adjusting for physiological factors and glucose area.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effects of physiological plasma insulin levels on glucose turnover parameters in familial hypercholesterolemia.

Eight young, non-obese patients with primary familial hypercholesterolemia (FH) and 8 healthy subjects matched for age, body mass index, lean body mass, plasma triglyceride and HDL-levels and arterial blood pressure were selected from a lipid clinic. Patients with FH had higher plasma LDL-cholesterol (8.3 +/- 0.5 vs. 4.1 +/- 0.2 mmol/l, P < 0.001) than controls but similar plasma triglyceride (1.15 +/- 0.04 vs. 1.10 +/- 0.02 mmol/l P = NS) levels. Both study groups were submitted to a euglycaemic hyperinsulinemic glucose clamp combined with simultaneous infusion of [3H]glucose to measure insulin action on whole-body glucose uptake and on hepatic glucose production. Two insulin infusion rates (0.15 mU/kg per min from 0 to 120 min and 0.30 mU/kg per min from 121 to 240 min) were used resulting in similar plasma insulin levels in both groups studied. Our results demonstrate that both whole-body glucose uptake and hepatic glucose output are similar in the fasting state as well as during insulin administration in both groups of subjects. We conclude that, in the absence of other causes of insulin resistance, isolated hypercholesterolemia is associated with normal sensitivity to insulin in both liver and peripheral tissues.

Adult↗