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Biomedical subjects

G Paolisso

Publications and source records attributed to G Paolisso.

At least 91 records · Page 5Linked to original sources

Congestive heart failure predicts the development of non-insulin-dependent diabetes mellitus in the elderly. The Osservatorio Geriatrico Regione Campania Group.

Congestive heart failure (CHF) is an insulin-resistant state which constitutes the main risk factor for the development of non-insulin-dependent diabetes mellitus (NIDDM). Our study investigated the predictive role of CHF on the development of NIDDM in 1,339 elderly subjects with a mean ( +/- SD) age of 74.2 +/- 6.4 years. CHF had a 9.5% prevalence, and 14.7% of the subjects had NIDDM. After stratification by age, subjects between 80 and 84 years had the highest prevalence of CHF and a total of 29.6% of CHF patients had NIDDM. In multiple logistic regression analysis, CHF was associated with NIDDM [odds ration (OR) = 2.0, 95% confidence interval (CI) - 1.6-2.5] independent of age, sex, family history of diabetes, body mass index, (BMI), waist/hip ratio, and diastolic blood pressure. When only untreated CHF patients were taken into account, the association between CHF and NIDDM was even stronger (OR = 4.0, 95% CI = 3.4-5.8). When untreated CHF patients were grouped into those with low (I and II) and high (III and IV) New York Heart Association (NYHA) classes, the association of CHF and NIDDM was stronger with the worsening of CHF. In a longitudinal study, CHF predicted NIDDM independently of age, sex, family history of diabetes, BMI, waist/hip ratio, systolic and diastolic blood pressure, and therapy for CHF (OR = 1.4, 95% CI = 1.1-1.8). CHF was associated with a higher prevalence of NIDDM and was a risk factor for its development. Elevated FFA concentrations may play a pivotal role.

Aged↗

Role of lipids in development of noninsulin-dependent diabetes mellitus: lessons learned from Pima Indians.

We studied the role of lipids in the pathogenesis of noninsulin-dependent diabetes mellitus (NIDDM) in Pima Indians. High plasma levels of nonesterified fatty acid (NEFA) predicted development of NIDDM, but this effect cannot entirely be explained by the glucose-fatty acid cycle. Dyslipidemia, although often associated with diabetes, did not seem to predict NIDDM and might rather be associated with, or the consequence of insulin resistance. In some individuals, a single amino acid substitution in the intestinal fatty acid binding protein could result in increased rates of intestinal absorption of dietary NEFA and thereby contribute to increased lipid-oxidation rates and insulin resistance.

Arizona↗

Hyperinsulinemia is associated with ventricular premature complexes.

The study investigated a possible association between fasting plasma insulin (FPI) levels and ventricular premature complexes (VPCs). One hundred eighty-six subjects without coronary artery disease (CAD), diabetes, hypertension, and left ventricular hypertrophy were recruited. All subjects underwent 24-hour electrocardiographic monitoring and oral glucose tolerance testing. The subjects were slightly overweight, normotensive, and nondiabetic. Subjects at the third tertile of FPI concentrations were the oldest and heaviest, with prevalent upper-body fat distribution, and had enhanced fasting plasma triglyceride and potassium concentrations, lower fasting plasma high-density lipoprotein (HDL) cholesterol concentration, and a greater number of VPCs versus subjects at the first and second tertiles. Independently of age, sex, body mass index (BMI), and waist to hip ratio (WHR), VPCs were correlated with FPI concentration (r = .19, P < .01). Multiple logistic regression analyses in which the presence or absence of VPCs was the dependent variable demonstrated that FPI concentrations were associated with VPCs independently of age, sex, BMI, WHR, daily physical activity (DPA), left ventricular mass index (LVMI), plasma low-density lipoprotein (LDL)/HDL cholesterol ratio, and triglyceride concentration (odds ratio [OR], 1.2; 95% confidence interval [CI], 1.0 to 1.6). After addition to the model of fasting plasma free fatty acids ([FFA] OR, 0.7; 95% CI, 0.6 to 1.3) or potassium (OR, 0.7; 95% CI, 0.6 to 1.1) concentrations, the association between FPI concentrations and VPCs is no longer significant. In conclusion, FPI concentrations are associated with VPCs in nondiabetic, normotensive, nonischemic subjects.

Adult↗

Glucose tolerance and insulin action in healthy centenarians.

Advancing age has been found to be associated with a decline in insulin action. Nevertheless, no study has been conducted in healthy centenarians. Our study investigates glucose tolerance and insulin action in centenarians. Fifty-two subjects were enrolled. The subjects were divided in three groups as follows: 1) adults (< 50 yr; n = 20);2) aged subjects (> 75 yr; n = 22); and 3) centenarians (> 100 yr; n = 14). Body composition was studied by bioimpedance analysis. In all subjects, an oral glucose tolerance test and euglycemic glucose clamp were performed. Centenarians have a lower fat-free mass (FFM) than aged subjects and adults, whereas fasting plasma glucose, triglycerides, free fatty acids, urea, and creatinine were not different in the groups studies. Centenarians had a 2-h plasma glucose concentration (6.0 +/- 0.2 mmol/l) that was lower than that in aged subjects (6.6 +/- 0.5 mmol/l, P < 0.05) but not different from adults [6.4 +/- 0.4 mmol/l, P = not significant (NS)]. During the clamp, plasma glucose and insulin concentrations were similar in the three groups. In these conditions, centenarians had a whole body glucose disposal (34.1 +/- 0.6 mumol.kg FFM-1.min 1) that was greater than that in aged subjects (23.3 +/- 0.5 mumol.kg FFM-1.min-1 P < 0.01) but not different from adults (34.6 +/- 0.5 mumol/kg x min, P = NS). In conclusion, our study demonstrates that centenarians compared with aged subjects had a preserved glucose tolerance and insulin action.

Adult↗

Does free fatty acid infusion impair insulin action also through an increase in oxidative stress?

In vitro studies have demonstrated that free fatty acids (FFA) may enhance oxidative stress. In contrast, no in vivo studies have addressed such a relationship. This four-part study aims at investigating the association between FFA and oxidative stress in healthy volunteers. The following experimental procedures were carried out: 1) determination and simple correlations among fasting plasma FFA, glucose, insulin, plasma thiobarbituric acid-reactive substance (TBARS), the ratio of reduced glutathione (GSH) to oxidized GSH, and lipid hydroperoxide (n = 30); 2) time-dependent effect of FFA on plasma TBARS concentrations and GSH/oxidized GSH ratio (n = 10); 3) dose-dependent effect of FFA on plasma TBARS concentrations (n = 9); and 4) relationship among plasma FFA concentrations, plasma TBARS concentrations, and insulin action (n = 11). The results demonstrate that fasting plasma FFA concentrations correlated with fasting plasma TBARS concentrations (r = 0.65; P < 0.001) and lipid hydroperoxide (r = 0.79; P < 0.001). The correlation between plasma FFA and TBARS remained significant even after adjustment for age, sex, body mass index, and fasting and 2-h plasma glucose concentrations (r = 0.43; P < 0.01). In the time-dependent study, plasma TBARS concentrations increased with the rise in plasma FFA concentrations. In the dose-response study, a progressive increase in fasting plasma FFA concentrations was achieved by varying the Intralipid infusion rate, which also caused plasma TBARS concentrations to increase progressively until they reached a plateau between the last two infusion rates (0.3 and 0.4 mL/min). A euglycemic hyperinsulinemic glucose clamp (insulin infusion rate, 10.2 pmol/kg min for 360 min) was also performed. Simultaneous 10% Intralipid (0.4 mL/min) infusion significantly enhanced plasma TBARS concentrations and inhibited insulin-stimulated whole body glucose disposal (WBGD). GSH infusion (15 mg/min for 360 min) had opposite effects on plasma TBARS concentrations and WBGD. A combined infusion of 10% Intralipid and GSH was associated with a stimulation of WBGD with a magnitude midway between that of 10% Intralipid and GSH infused separately. In conclusion, fasting plasma FFA seems to enhances oxidative stress, which might contribute to the disruptive effects of plasma FFA on insulin-mediated glucose uptake.

Adult↗

Insulin action and age. European Group for the Study of Insulin Resistance (EGIR).

Evidence that age is associated with insulin resistance is discordant. We analyzed euglycemic insulin clamp (1 mU x min(-1) x kg(-1)) data collected at 20 centers throughout Europe from 1,146 men and women with normal glucose tolerance, ranging in age from 18 to 85 years. In the whole group, insulin action (as the M value) declined slightly with age (at a rate of 0.9 micromol x min(-1)-kg(-1) per decade of life, 95% CI = 0.4-1.3, P = 0.0002). When adjusted for BMI, this relationship was no longer statistically significant. The same result was obtained whether insulin action was expressed per kilogram of body weight or per kilogram of fat-free mass, expressed as the M:I ratio, or estimated from fasting plasma insulin concentrations. Subgroup analysis showed that a significant BMI-adjusted decrease in insulin action with age was present only in lean (BMI <25 kg/m2) women (a rate of 1.6 micromol x min(-1) x kg(-1) per decade, 95% CI = 0.6-2.5, P = 0.001), in whom percentage fat mass also increased with age (by 0.38% body weight per decade, P = 0.0007). Insulin action was positively associated with insulin suppression of circulating free fatty acids (FFAs) (+1.5 micromol x min(-1) x kg(-1) for each 10% increase in FFA suppression, P < 0.0001) in a multivariate model accounting for sex, BMI, age, and fasting FFA levels. Furthermore, insulin suppression of FFAs improved with age in men (2% per decade, P < 0.0001) but not in women. In the subgroup of lean women in whom insulin action declined with age, adding FFA suppression to a multiple regression equation canceled the association between age and insulin action. Thus, the small effect of age on insulin action could be adequately explained on the basis of age-related changes in body composition and substrate competition. We conclude that in healthy Europeans, age per se is not a significant cause of insulin resistance of glucose metabolism or lipolysis.

Adult↗

Oxidative stress and diabetic vascular complications.

Long-term vascular complications still represent the main cause of morbidity and mortality in diabetic patients. Although prospective randomized long-term clinical studies comparing the effects of conventional and intensive therapy have demonstrated a clear link between diabetic hyperglycemia and the development of secondary complications of diabetes, they have not defined the mechanism through which excess glucose results in tissue damage. Evidence has accumulated indicating that the generation of reactive oxygen species (oxidative stress) may play an important role in the etiology of diabetic complications. This hypothesis is supported by evidence that many biochemical pathways strictly associated with hyperglycemia (glucose autoxidation, polyol pathway, prostanoid synthesis, protein glycation) can increase the production of free radicals. Furthermore, exposure of endothelial cells to high glucose leads to augmented production of superoxide anion, which may quench nitric oxide, a potent endothelium-derived vasodilator that participates in the general homeostasis of the vasculature. In further support of the consequential injurious role of oxidative stress, many of the adverse effects of high glucose on endothelial functions, such as reduced endothelial-dependent relaxation and delayed cell replication, are reversed by antioxidants. A rational extension of this proposed role for oxidative stress is the suggestion that the different susceptibility of diabetic patients to microvascular and macrovascular complications may be a function of the endogenous antioxidant status.

Diabetes Mellitus, Type 1↗

Non-insulin-dependent diabetes mellitus is associated with a greater prevalence of depression in the elderly. The Osservatorio Geriatrico of Campania Region Group.

We investigated the association of non-insulin-dependent (Type 2) diabetes mellitus and depression symptoms in a representative community-dwelling elderly population independently of other conditions such as gender, age, status, disability, cognitive impairment and a number of chronic medical conditions such as chronic obstructive lung disease, degenerative joint disease, heart disease, cirrhosis of the liver, cholelithiasis, peptic ulcer and kidney stones. A total of 1339 elderly subjects living in southern Italy were randomly selected from electoral rolls and evaluated. All subjects were tested by the Geriatric Depression Scale to detect depression, the Mini-Mental State Examination to study cognitive function and the Activity Daily Living Index to evaluate disability. Non-insulin-dependent diabetes mellitus affected 14.7% of our sample. Depression was more prevalent in women over 75 years of age than in younger women (15.9 vs 8.1%, p < 0.001). In multiple linear regression analysis, diabetes mellitus was found to be significantly associated with depression independently of age, gender, loneliness, cognitive impairment, chronic obstructive lung disease, degenerative joint disease, heart diseases, cancer, kidney disease, cirrhosis of the liver and cholelithiasis. It is concluded that non-insulin-dependent diabetes mellitus is significantly associated with depression in the elderly, which may have clinical implications for the achievement of sufficient blood glucose control.

Aged↗

Exhaustion of blood glucose response and enhancement of insulin response after repeated glucagon injections in type-2 diabetes: potentiation by progressive hyperglycemia.

AIMS: To investigate the hyperglycemic and insulinemic response to repeated glucagon injections in Type-2 (non-insulin-dependent) diabetic patients. METHODS: In overnight fasted Type-2 diabetic patients, three i.v. glucagon (1 mg) injections were given as a bolus at two-hour intervals. In the hour preceding each glucagon injection, 6 patients received saline and they were tested at near-baseline blood glucose levels, while 8 patients received a glucose-controlled glucose infusion and they were tested at increasing blood glucose levels (7.5 +/- 0.2, 12.9 +/- 0.5 and 18.7 +/- 0.7 mmol/l). Blood samples were collected at 0, 3, 5, 10, 15, 30 and 60 min after each glucagon injection. RESULTS: In the patients tested at near-baseline blood glucose levels, the blood glucose rise induced by glucagon was smaller after repeated injections. By contrast, the B-cell response to glucagon was well preserved. In the patients tested at increasing blood glucose levels, the blood glucose response to glucagon was abolished after repeated injections. By contrast, the B-cell response was significantly potentiated. The respective areas under the curve of plasma insulin levels in response to glucagon were 563 +/- 72, 1047 +/- 154 and 1844 +/- 305 m U x 30 min/l (p < 0.001). CONCLUSION: In Type-2 (non-insulin-dependent) diabetic patients, repeated glucagon injections, even when administered in a short (4 h) period of time, do not exhaust the B-cell. Endogenous insulin secretion is even potentiated at increasing blood glucose levels. By contrast, the hyperglycemic response to glucagon is significantly abolished, particularly at high blood glucose levels.

Aged↗

Low-dose Iloprost infusion improves insulin action and non-oxidative glucose metabolism in hypertensive patients.

Fourteen hypertensive (174.3/98.3 mmHg) non-diabetic patients were given a euglyceamic glucose clamp along with infusion of 0.9% NaCl and the prostacyclin (PGI2) analogue Iloprost (0.7 ng x kg x min(-1)). Substrate oxidation was also determined by indirect calorimetry. Over the last 60 min of the clamp, Iloprost vs saline improved whole body glucose disposal (WBGD) (35 vs 28.3 micromol x kg(-1) LBM) and non-oxidative glucose metabolism (24.7 vs 18.1 micromol x kg(-1) LBM x min(-1). Iloprost delivery was associated with a significant decrease in membrane microviscosity (0.253 vs 0.205), but did not affect arterial blood pressure and heart rate. In nine patients, skeletal muscle blood flow (SMBF) and insulin-stimulated glucose uptake (GU) were also studied. At the end of the study, despite a similar SMBF (37 vs 38 ml x min(-1) x kg(-1)), GU (0.55 vs 0.46 mmol x l(-1)) was significantly increased by Iloprost infusion. Percentage decrease in membrane microviscosity was correlated with percentage increase in WBGD (r = 0.65) and non-oxidative glucose metabolism (r = 0.68). In conclusion, low-dose Iloprost infusion improves insulin action and non-oxidative glucose metabolism in hypertensive patients.

Blood Glucose↗

Opposite effects of short- and long-term fatty acid infusion on insulin secretion in healthy subjects.

Our study investigates short- and long-term effects of infusion of non-esterified fatty acids (NEFA) on insulin secretion in healthy subjects. Twelve healthy individuals underwent a 24-h Intralipid (10% triglyceride emulsion) infusion at a rate of 0.4 ml/min with a simultaneous infusion of heparin (a bolus of 200 U followed by 0.2 U/min per kg body weight). After an overnight fast (baseline), at 6 and at 24 h of Intralipid infusion and 24 h after Intralipid discontinuation (recovery test), all subjects underwent an intravenous glucose tolerance test (iv-GTT) (25 g of glucose/min). Intralipid infusion caused a threefold rise in plasma NEFA concentrations with no difference between the 6- and the 24-h concentrations. Compared to baseline acute insulin response (AIR) (AIR = 63 +/- 8 mU/l), short-term (6-h) Intralipid infusion was associated with a significant increase in AIR (86 +/- 12 mU/l p < 0.01); in contrast, long-term (24-h) Intralipid delivery was associated with inhibition of AIR (31 +/- 5 mU/l) compared to baseline (p < 0.001) and to the 6-h (p < 0.03) triglyceride emulsion infusion. Intralipid infusion was associated with a progressive and significant decline in respiratory quotient (RQ). A positive correlation between changes in fasting plasma NEFA concentrations and AIR at the 6-h infusion (r = 0.89 p < 0.001) was found. In contrast, at the end of the Intralipid infusion period, changes in plasma NEFA concentrations and AIR were negatively correlated (r = -0.87 p < 0.001). The recovery test showed that fasting plasma NEFA concentrations, RQ and AIR had returned to baseline values. In the control study (n = 8) 0.9% NaCl infusion did not mimick the effect of Intralipid. In conclusion, our study demonstrates that short- and long-term exposures of beta cells to high plasma NEFA concentrations have opposite effects on glucose-induced insulin secretion.

Adult↗

A high concentration of fasting plasma non-esterified fatty acids is a risk factor for the development of NIDDM.

To assess the role of fasting plasma non-esterified fatty acids (NEFA) in the development of non-insulin-dependent diabetes mellitus (NIDDM), data were analysed from annual examinations of 190 non-diabetic Pima Indians. Glucose tolerance was measured by a 75-g oral glucose tolerance test, insulin action by a euglycaemic hyperinsulinaemic (40 mU x m-2 x min-1) clamp and in vitro lipolysis using isolated abdominal fat cells. After a mean follow-up period of 4.0 +/- 2.4 years (mean +/- SD), 47 subjects developed NIDDM. Risk factors for NIDDM were estimated by proportional-hazards analysis and risk ratios (RR) with 95% confidence intervals (95% CI) calculated at the 90th and 10th percentile of the predictor variables. A large average fat-cell volume was predictive of NIDDM (RR=2.4; 95% CI=1.2-4.8) independent of age, sex, percent body and body fat distribution. A high fasting plasma NEFA concentration was also a risk factor for NIDDM (RR=2.3; 95% CI=1.1-4.7) independent of sex, percent body fat, waist/thigh ratio, insulin-mediated glucose uptake and fasting triglyceride concentration. We conclude that large fat cells and the resulting increased plasma NEFA concentrations are risk factors for the development of NIDDM.

Adipocytes↗

Diabetes mellitus, hypertension, and cardiovascular disease: which role for oxidative stress?

Accelerated atherosclerotic vascular disease is the leading cause of mortality in patients with diabetes mellitus. Endothelium-derived nitric oxide (NO) is a potent endogenous nitrovasodilator and plays a major role in modulation of vascular tone. Selective impairment of endothelium-dependent relaxation has been demonstrated in aortas of both nondiabetic animals exposed to elevated concentrations of glucose in vitro and insulin-dependent diabetic animals. The impaired NO release in experimentally induced diabetes may be prevented by a number of antioxidants. It has been hypothesized that oxygen-derived free radicals (OFR) generated during both glucose autoxidation and formation of advanced glycosylation end products may interfere with NO action and attenuate its vasodilatory activity. The oxidative injury may also be increased in diabetes mellitus because of a weakened defense due to reduced endogenous antioxidants (vitamin E, reduced glutathione [GSH]). A defective endothelium-dependent vascular relaxation has been found in animal models of hypertension and in hypertensive patients. An imbalance due to reduced production of NO or increased production of free radicals, mainly superoxide anion, may facilitate the development of an arterial functional spasm. Treatment with different antioxidants increases blood flow in the forearm and decreases blood pressure and viscosity in normal humans; vitamin E inhibits nonenzymatic glycosylation, oxidative stress, and red blood cell microviscosity in diabetic patients. Long-term randomized clinical trials of adequate size in secondary and primary prevention could support the free-radical hypothesis for diabetic diabetic vascular complications and the use of antioxidants to reduce the risk of coronary heart disease.

Animals↗

Morpho-functional assessment of interatrial septum: a transesophageal echocardiographic study.

BACKGROUND: Despite the increasing number of reports on lipomatous hypertrophy of interatrial septum, a standardization of measurement of the dimensions of the interatrial septum (IAS) in the different phases of cardiac cycle has not been reported. Moreover, no data on modification of thickness with age and in specific cardiac diseases are available. OBJECTIVE: Our purpose was to study whether the changes of thickness and thinning of IAS may be related to age, left atrial dimension, cardiac cycle and different cardiac diseases. METHODS: 248 patients (mean age 52.7 +/- 19.9 years) underwent transthoracic (TTE) and transesophageal (TEE) echocardiography. IAS was measured at the constant regions anterior and posterior to the fossa ovalis. IAS thickness (tk), thinning (th) and % thinning (% th) were measured. RESULTS: IAS thickness ranged from 4 to 13 mm at the time of ventricular end-systolic phase (mean 6.7 +/- 1.9 mm) and from 6 to 16 mm at the time of atrial systole (mean 9.9 +/- 1.8 mm); significant statistical difference between these values was found (P < 0.01). IAS thinning ranged from 1 to 7 mm (mean 3.42 +/- 1.8) while % IAS thinning from 18 to 76% (mean 36.53 +/- 16.36%). Statistical analysis showed a significant positive correlation between age and ventricular end-systolic thickness and atrial systolic thickness and thinning. An insignificant correlation was found between age and % IAS thinning and between left atrial dimension and IAS tk and th. CONCLUSIONS: Our results demonstrate that IAS thickness increases by age; no correlation exists between IAS thinning and age. There is no difference between IAS thickness and thinning in patients with or without cardiac disease. We believe that the thickness of IAS can be considered hypertrophic only if it exceeds the value of 15 mm during both ventricular end-systolic and atrial systolic phases of the cardiac cycle. IAS thickness and thinning might be an additional parameter to evaluate systolic atrial function particularly with regard to maintenance of synus rhythm after conversion from atrial fibrillation as well as to better understand its role in determining the filling of ventricles in different clinical conditions.

Adolescent↗

Metabolic benefits deriving from chronic vitamin C supplementation in aged non-insulin dependent diabetics.

OBJECTIVE: Our study investigated the metabolic benefits deriving from chronic pharmacological vitamin C administration in aged non-insulin dependent (Type II) diabetic patients. METHODS: Forty type II diabetic patients (age: 72 +/- 0.5 years) underwent placebo and vitamin C (0.5 g twice daily) administration in double-blind, randomized, cross-over fashion. All patients were treated by oral hypoglycaemic agents which continued throughout the study. After baseline observations, treatment periods lasted 4 months and were separated by a 30-day wash-out period. RESULTS: Patients' antropometric data were unchanged throughout the study. Chronic vitamin C administration vs placebo was associated with a significant decline in fasting plasma free radicals (0.26 +/- 0.06 vs 0.49 +/- 0.07 p < 0.03) and insulin (90 +/- 4 vs 73 +/- 6 pmol/L p < 0.04), total- (7.3 +/- 0.5 vs 5.8 +/- 0.4 mmol/L p < 0.03), LDL-cholesterol (5.6 +/- 0.6 vs 4.1 +/- 0.3 mmol/L p < 0.05) and triglycerides (2.58 +/- 0.07 vs 2.08 +/- 0.04 mmol/L p < 0.04) levels. In 20 patients, chronic vitamin C administration improved whole body glucose disposal and nonoxidative glucose metabolism. Percent increase in plasma vitamin C levels correlated with the percent decline in plasma LDL-cholesterol (r = 0.44; p < 0.007) and insulin levels (r = 0.42; p < 0.006). Finally percent increase in plasma vitamin C levels was correlated with the percent decline in plasma free radicals and increase in GSH levels. CONCLUSIONS: Chronic vitamin C administration has beneficial effects upon glucose and lipid metabolism in aged non-insulin dependent (type II) diabetic patients.

Aged↗

Chronic intake of pharmacological doses of vitamin E might be useful in the therapy of elderly patients with coronary heart disease.

Thirty elderly (mean +/- SEM: 73.8 +/- 2.1 y) nondiabetic, moderately obese (body mass index = 28.3 +/- 0.6 kg/m2) patients with stable effort angina underwent an oral-glucose-tolerance test and a euglycemic hyperinsulinemic glucose clamp before and after vitamin E supplementation (900 mg/d for 4 mo). The study was of a randomized, placebo-controlled, double-blind, and crossover design. Anthropometric indexes were stable throughout the study. Despite similar fasting and 2-h plasma glucose concentrations, vitamin E administration (compared with placebo) lowered fasting (88 +/- 14 and 68 +/- 9 pmol/L, P < 0.02) and 2-h (348 +/- 43 and 263 +/- 28 pmol/L, P < 0.05) plasma insulin concentrations, plasma triglyceride concentrations (1.34 +/- 0.06 and 1.07 +/- 0.03 mmol/L, P < 0.05), and the ratio of plasma LDL to HDL cholesterol (7.64 +/- 0.31 and 5.52 +/- 0.38, P < 0.02). Vitamin E administration was associated with higher nonoxidative glucose metabolism (18.1 +/- 0.5 and 10.6 +/- 0.7 mumol.kg lean body mass-1.min-1, P < 0.03) than was placebo administration during the euglycemic glucose clamp. We conclude that chronic intake of pharmacological doses of vitamin E might be useful in the therapy of elderly insulin-resistant patients with coronary heart disease.

Aged↗

Body composition, body fat distribution, and resting metabolic rate in healthy centenarians.

Our study investigated body composition and body fat distribution in healthy centenarians. Body composition, body fat distribution, and resting metabolic rate (RMR) were studied in 40 adult subjects aged < 50 y, 35 aged subjects > 75 y, and 15 healthy centenarians aged > 100 y. Body composition was determined by bioimpedance analysis, body fat distribution was calculated as waist-hip ratio (WHR), and RMR was calculated by using the Arciero-Poehlman formula. Healthy centenarians had a cognitive impairment and degree of disability greater than aged subjects. Despite such differences, fat-free mass (FFM) and RMR were not different in centenarians compared with aged subjects but were lower than in adult subjects. In contrast, healthy centenarians had a WHR lower than that of aged subjects but not different from that of the adult subjects. After the level of physical activity and degree of disability were adjusted for, FFM (44 +/- 2.7 and 40 +/- 1.1 kg; P < 0.05) and RMR (6757 +/- 761 and 5891 +/- 723 kJ/24 h; P < 0.05) were significantly higher in healthy centenarians than in aged subjects, respectively. Independent of age, sex, body weight, degree of disability, level of physical activity, and fasting plasma triiodothyronine, there was a strong correlation between RMR and FFM (r = 0.50, P < 0.05) in healthy centenarians. In conclusion, healthy centenarians had a lower FFM and higher body fat content than aged subjects. Level of physical activity and degree of disability seem to be the major determinants for explaining such differences.

Adipose Tissue↗