Search PubMed⌕ Search

Biomedical subjects

A Golay

Publications and source records attributed to A Golay.

At least 127 records · Page 7Linked to original sources
PubMed1986

Lack of thermogenic response to glucose/insulin infusion in diabetic obese subjects.

The change in energy expenditure consecutive to the infusion of glucose/insulin was examined in 17 non-obese (ten young, seven middle-aged) and 27 diabetic and non-diabetic obese subjects by employing the euglycemic insulin clamp technique in conjunction with continuous indirect calorimetry. The obese subjects were divided into four groups according to their response to a 100-g oral glucose test: group A, normal glucose tolerance; group B, impaired glucose tolerance; group C, diabetes with increased insulin response; group D, diabetes with reduced insulin response. The glucose/insulin infusion provoked an increase in energy expenditure in both young and middle-aged controls (+8.2 +/- 1.3 percent and +5.9 +/- 0.5 percent over the preinfusion baseline respectively), but a lower increase in the non-diabetic obese groups A and B (+4.0 +/- 0.7 percent and +2.0 +/- 1.0 percent over the preinfusion baseline respectively, P less than 0.05 and P less than 0.01 vs young controls). However, in the diabetic obese groups C and D, energy expenditure failed to increase in response to the glucose/insulin infusion (mean change: +0.1 +/- 1.0 percent and -2.0 +/- 1.9 percent (P less than 0.01, vs middle-aged) over the preinfusion baseline respectively). When the glucose-induced thermogenesis (GIT) was related to the glucose uptake--taking into account the hepatic glucose production--the GIT was found to be similarly reduced in the diabetics groups (C and D). The net change in the rate of energy expenditure was found to be significantly correlated with the rate of glucose uptake (r = +0.647, n = 44, P less than 0.001) when all the individuals were pooled. In conclusion, this study shows that the low glucose-induced thermogenesis in obese diabetics during glucose insulin infusion is mainly related to a reduced rate of glucose uptake; in addition, inhibition of gluconeogenesis by the glucose/insulin infusion may also contribute to decrease the thermogenic response.

Adult↗
PubMed1986

Effect of trestatin, a new inhibitor of pancreatic alpha-amylase, on starch metabolism in man.

The effect of two doses (3 mg and 10 mg) of the inhibitor of pancreatic alpha-amylase trestatin on the metabolism of an oral load of 75 g of starch was observed in healthy human subjects. The mean elevation of plasma glucose over the 4 h following the load was markedly reduced both with 10 mg (mean +/- s.e.m.: 1.4 +/- 1.2 mg/dl) and with 3 mg of trestatin (7.2 +/- 2.0 mg/dl) when compared to placebo (19.5 +/- 5.1 mg/dl) (P less than 0.01 in both cases). The mean elevation of plasma insulin was decreased with both 10 mg (mean +/- s.e.m.: 1 +/- 1 microU/ml) and 3 mg of trestatin (6 +/- 2 microU/ml) when compared to placebo (20 +/- 4 microU/ml) (P less than 0.01 in both cases). Suprabasal glucose oxidation, measured by indirect calorimetry, was markedly decreased by trestatin (mean +/- s.e.m.: 2.5 +/- 1.1 g/4 h with 10 mg of trestatin versus 12.0 +/- 2.0 g/4 h with placebo, P less than 0.001). To examine whether trestatin had any action on alpha-1-4 glycosidase activity, an oral load of 100 g sucrose together with either 50 mg trestatin or with a placebo was administered to four healthy human subjects. Trestatin was observed to have only few effects on plasma glucose and insulin levels following sucrose ingestion. This suggests that its main site of action is at the alpha-amylase level. Breath hydrogen was shown to increase after ingestion of starch plus trestatin at the two doses studied. It is concluded that trestatin is a powerful inhibitor of pancreatic alpha-amylase which could be of great help in the dietary management of diabetic patients.

Adult↗
PubMed1985

Evidence for diminished brain 5-hydroxytryptamine biosynthesis in obese diabetic and non-diabetic humans.

Obese persons are often reported to have marked cravings for simple carbohydrate-rich foods. Because of the proposed relationships between protein/carbohydrate selection, plasma tryptophan (TRP) to large neutral amino acids (LNAA) ratios, and brain 5-hydroxytryptamine (5-HT) neurotransmission, we examined the plasma TRP/LNAA ratios in four categories of obese subjects, before and 120 min after oral glucose tolerance test (GTT). Plasma TRP/LNAA ratios were reduced in obese, non-diabetics by 18%, the same extent as for older (approximately 52 yr old) nonobese subjects. In more advanced obesity, ie obesity associated either with glucose intolerance, hyperinsulinemia or hypoinsulinemia, plasma TRP/LNAA ratios were reduced by 25%. One hundred twenty minutes after a 100 g glucose load plasma TRP/LNAA had not been normalized. Based on animal data, these results suggest there may be diminished 5-HT neurotransmission in obese diabetics. The implications of these findings for the cravings of obese for carbohydrate-rich foods is discussed.

Adolescent↗
PubMed1985

Effect of weight loss on glucose disposal in obese and obese diabetic patients.

The purpose of the study was to examine the effect of short-term weight loss on glucose disposal and lipid oxidation in obese patients. Twenty-six obese patients were divided into three groups according to their degree of glucose intolerance: normal glucose tolerance = Gp I; impaired glucose tolerance without diabetes = Gp II; diabetes = Gp III. The patients submitted to an hypocaloric, high-protein diet for 8 to 45 weeks. Respiratory exchange measurements were performed by means of continuous indirect calorimetry during a 100 g, 3 h oral glucose tolerance test (OGTT) before weight loss and were repeated at the end of the weight loss period, 3 to 8 weeks after the reintroduction of a balanced isocaloric diet. Glucose tolerance, which was decreased in Gps II and III, improved after weight loss. Glucose oxidation, which was decreased in Gps II and III showed improvement after weight reduction in both Gp II (30.9 +/- 2.3 after weight loss vs 24.2 +/- 2.0 g/3 h before, P less than 0.025) and in Gp III (33.1 +/- 1.6 vs 25.8 +/- 4.1, ns). In the diabetic group (Gp III), before weight loss, a decrease in nonoxidative glucose uptake was observed, which was probably due both to a decrease in glucose storage and to the inhibition of splanchnic glucose output. After weight loss, it increased significantly from 27.7 +/- 5.2 to 56.9 +/- 2.3 g/3 h (P less than 0.001). Postabsorptive plasma insulin levels decreased in all groups following weight reduction. When exaggerated the insulin response to the glucose load fell to normal values whereas the insulin response increased in the diabetic patients in whom it was initially blunted. Lipid oxidation rates, both preload and postload, were markedly elevated before weight loss in all three groups. They were substantially reduced after weight loss. This study shows that a weight loss of 10 to 33 kg in obese patients promoted an increase in the subnormal glucose oxidation rate in Gp II as well as an improvement of the low nonoxidative glucose uptake in the diabetic group, thus improving their glucose tolerance. There was a simultaneous reduction in lipid oxidation in both groups. Furthermore, the insulin response to the glucose load, whether elevated or decreased before weight loss, tended towards normalization after weight reduction.

Adult↗
PubMed1984

[Metabolic effects of gliclazide in diabetes type II patients. Study with indirect calorimetry].

An attempt is made to determine the effect of treatment with gliclazide on the manner in which obese patients with noninsulin-dependent diabetes dispose of an oral glucose load. Six patients were studied on two occasions - once after one month of an isocaloric diet containing 40% carbohydrate, and two months after gliclazide had been added. Body weight remained constant throughout the three months. However, fasting plasma glucose concentration fell and mean (+/- SEM) incremental insulin response to oral glucose increased significantly (p less than 0.05) with drug therapy (51.1 +/- 14.6 microU/ml vs 17.1 +/- 1.5 microU/ml). Glucose oxidation significantly improved after gliclazide treatment (16.9 +/- 2.4 g/3 h vs 7.5 +/- 2.1 g/3 h, p less than 0.02) in parallel with the fall in plasma glucose and the increase in insulin response. In addition, glucose storage significantly increased after drug therapy (44.1 +/- 10.1 g/3 h vs 28.4 +/- 7.2 g/3 h, p less than 0.001). In contrast, lipid oxidation fell with gliclazide treatment (7.2 +/- 0.7 g/2 h vs 12.0 +/- 1.7 g/3 h, p less than 0.02). This effect may be explained by improvement of the antilipolytic effect of insulin. In conclusion, improvement in glucose oxidation (25%) and in glucose storage (55%), together with reduced lipid oxidation, was observed after two months of gliclazide therapy.

Blood Glucose↗
PubMed1984

Study on lipid metabolism in obesity diabetes.

Knowing the relationship between obesity and diabetes, the purpose of our work was to study the alterations in lipid metabolism as measured by continuous indirect calorimetry in the course of a 100-g oral glucose-tolerance test in groups of obese patients without and with diabetes, respectively. Seventy-nine obese patients participated in the study. They were divided into four groups according to the degree of carbohydrate intolerance: group A, normal glucose tolerance; group B, impaired glucose tolerance; group C, diabetes with hyperinsulinemic response to the load; group D, diabetes with impaired insulin response. All four groups of patients presented an increase in lipid oxidation, both in the fasting state and during the three-hour glucose tolerance test, when compared to the control group. The lipid oxidation rate was roughly parallel to plasma free fatty acid (FFA) levels. The contribution of lipids to energy expenditure was higher in obese as compared to control subjects. These observations suggest that the larger part taken by lipids in the energy metabolism of both nondiabetic and diabetic obese humans is a consequence of their increased fat stores and that the resulting decrease in carbohydrate metabolism may lead, as a late consequence, to alterations in glucose tolerance. The latter may result in delayed glucose storage and oxidation in the obese patient.

Adult↗
PubMed1984

Decreased glucose-induced thermogenesis after weight loss in obese subjects: a predisposing factor for relapse of obesity?

Glucose-induced thermogenesis (GIT) after a 100-g oral glucose load was measured by continuous indirect calorimetry in 32 nondiabetic and diabetic obese subjects and compared to 17 young and 13 middle aged control subjects. The obese subjects were divided into three groups: A (n = 12) normal glucose tolerance, B (n = 13) impaired glucose tolerance, and C (n = 7) diabetics, and were studied before and after a body weight loss ranging from 9.6 to 33.5 kg consecutive to a 4 to 6 months hypocaloric diet. GIT, measured over 3 h and expressed as percentage of the energy content of the load, was significantly reduced in obese groups A and C (6.2 +/- 0.6, and 3.8 +/- 0.7%, respectively) when compared to their age-matched control groups: 8.6 +/- 0.7 (young) and 5.8 +/- 0.3% (middle aged). Obese group B had a GIT of 6.1 +/- 0.6% which was lower than that of the young control group but not different from the middle-aged control group. After weight loss, GIT in the obese was further reduced in groups A and B than before weight loss: ie, 3.4 +/- 0.6 (p less than 0.001), 3.7 +/- 0.5 (p less than 0.01) respectively, whereas in group C, weight loss induced no further diminution in GIT (3.8 +/- 0.6%). These results support the concept of a thermogenic defect after glucose ingestion in obese individuals which is not the consequence of their excess body weight but may be one of the factors favoring the relapse of obesity after weight loss.

Adult↗
PubMed1984

Effect of beta and alpha adrenergic blockade on glucose-induced thermogenesis in man.

After intravenous glucose/insulin infusion there is an increase in oxygen consumption and energy expenditure that has been referred to as thermogenesis. To examine the contribution of the beta and alpha adrenergic nervous system to this thermogenic response, 12 healthy volunteers participated in three studies: (a) euglycemic insulin (plasma insulin approximately 100 microunits/ml) clamp study (n = 12); (b) insulin clamp study after beta adrenergic blockade with intravenous propranolol for 1 h (n = 12); (c) insulin clamp study after alpha adrenergic blockade with phentolamine for 1 h (n = 5). During the control insulin clamp study total glucose uptake, glucose oxidation and nonoxidative glucose uptake averaged 7.85 +/- 0.47, 2.62 +/- 0.22, and 5.23 +/- 0.51 mg/kg X min. After propranolol infusion, insulin-mediated glucose uptake was significantly reduced, 6.89 +/- 0.41 (P less than 0.02). This decrease was primarily the result of a decrease in glucose oxidation (1.97 +/- 0.19 mg/kg X min, P less than 0.01) without any change in nonoxidative glucose metabolism. Phentolamine administration had no effect on total glucose uptake, glucose oxidation, or nonoxidative glucose disposal. The increments in energy expenditure (0.10 +/- 0.01 vs. 0.03 +/- 0.01 kcal/min) and glucose/insulin-induced thermogenesis (4.9 +/- 0.5 vs. 1.5 +/- 0.5%) were reduced by 70% during the propranolol/insulin clamp study. The increments in energy expenditure (0.12 +/- 0.03 kcal/min) and thermogenesis (5.0 +/- 1.5%) were not affected by phentolamine. These results indicate that activation of the beta adrenergic receptor plays an important role in the insulin/glucose-mediated increase in energy expenditure and thermogenesis. In contrast, the alpha adrenergic receptor does not appear to participate in this response.

Adult↗
PubMed1983

Stimulation of thermogenesis in men after combined glucose-long-chain triglyceride infusion.

The effect of combined long-chain triglyceride infusion (Intralipid 20%) with graded doses of insulin/glucose on energy expenditure was examined in 17 healthy young male volunteers by using the euglycemic insulin clamp technique in combination with indirect calorimetry. Intralipid was infused for 90 min at a constant rate of 0.23 g/min; plasma free fatty acids increased from base-line values of 380 +/- 8 mumol/l to steady state levels of 650 +/- 12 mumol/l. After 90 min the Intralipid was continued and insulin was infused at three rates (0.5, 2, and 4 mU/kg . min) to achieve steady state hyperinsulinemic plateaus of 63 +/- 4, 167 +/- 10, and 410 +/- 15 microU/ml. Plasma glucose concentration was maintained constant at basal euglycemic levels (insulin clamp technique) by infusing glucose at 0.24, 0.48, and 0.59 g/min, respectively. Glucose storage during the insulin clamp (ie, glucose uptake minus glucose oxidation) was 0.13, 0.33, and 0.40 g/min for each group and exogenous lipid storage was 0.17, 0.18, and 0.19 g/min, respectively. The net increment in energy expenditure was 0.15, 0.24, and 0.26 kcal/min, respectively, which represents 8.5% of the energy content of the total amount of glucose and lipid stored. The experimentally determined value (approximately 9%) for the cost of storing both glucose and lipid was found to be significantly greater than predicted by stoichiometric calculations. However, the experimental value for the combined infusion was less than that observed for glucose storage alone (12%). This finding provides support for the use of combined glucose/fat infusions in parenteral nutrition as it is used more economically than when glucose is infused alone.

Adult↗
PubMed1983

Decreased thermogenic response to an oral glucose load in older subjects.

The thermogenic response to a 100 g oral glucose load was studied by indirect calorimetry in 13 older persons (age range, 38-68 years) and compared with that of 16 young matched controls of similar body weight (age range, 19-30 years). The glucose-induced thermogenesis measured over 180 min and expressed as a per cent of the energy content of the glucose load was found to be reduced in the older subjects, i.e., 5.8 +/- 0.3 per cent vs 8.6 +/- 0.7 per cent, P less than 0.002). This was also accompanied by a significant decrease in the glucose oxidation rate when averaged over the same three-hour period following the glucose load, i.e., 153 mg/min vs 213 mg/min in the control subjects (P less than 0.001) despite a similar time course of glycemia. This study suggests that the thermogenic response to an oral glucose load is blunted in older people, and this may represent an additional factor that contributes to the decreased energy requirement with age and therefore to the increased propensity to obesity if energy intake is not adjusted.

Adult↗
PubMedDate not supplied

Comparison of metabolic effects of white beans processed into two different physical forms.

In the present study eight control subjects and eight patients with non-insulin-dependent diabetes mellitus (NIDDM) consumed single portions of processed beans equivalent to 50 g of carbohydrate. The beans were processed by different methods into two physical forms; one maintained the integrity of the bean cells (undamaged bean cells, UC) and the other ruptured the bean cells (damaged bean cells, DC). Incremental glucose response areas after ingestion of either UC or DC were not significantly different in control subjects, while incremental insulin response areas (49 +/- 7 vs. 26 +/- 4 microU X ml-1 X h-1, P less than .05) were significantly lower after eating UC-processed beans. In patients with NIDDM both incremental glucose (150 +/- 14 vs. 73 +/- 25 mg X dl-1 X h-1, P less than .001) and insulin (67 +/- 16 vs. 46 +/- 11 microU X ml-1 X h-1, P less than .05) response areas were significantly lower after UC administration. To test the effectiveness of the UC-processed bean when incorporated into mixed meals, nine patients with NIDDM consumed mixed meals containing either DC or UC on two separate mornings. The test meals represented a typical Mexican American use of pureed beans wrapped in a flour tortilla topped with melted cheese. Incremental glucose responses were significantly lower after the UC meal (171 +/- 42 mg X dl-1 X h-1, P less than .05) when compared with the DC meal (212 +/- 34 mg X dl-1 X h-1). Incremental insulin areas were also lower after the UC (91 +/- 19 microU X ml-1 X h-1) when compared with the DC meal (120 +/- 22 microU X ml-1 X h-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Interaction of lipid and carbohydrate metabolism after infusions of lipids or of lipid lowering agents: lack of a direct relationship between free fatty acid concentrations and glucose disposal.

The present work was planned to study the effects of changes in lipid metabolism irrespective of FFA concentrations (FFA) on the regulation of oxidative and nonoxidative disposal of a glucose infusion during hyperinsulinaemia. Fifteen normal volunteers participated in the 3 protocols, in which 1) Intralipid 2) beta-pyridylcarbinol or 3) isotonic saline were infused during 2 hours. Thereafter, these infusions were discontinued and a two-hour euglycaemic hyperinsulinaemic clamp was performed. All three studies were carried out in combination with indirect calorimetry to measure glucose uptake, and oxidative and nonoxidative glucose disposal (corresponding essentially to glucose storage). Plasma FFA concentrations were 508 +/- 34, 601 +/- 43 and 546 +/- 45 mumol/l in the basal state during the Intralipid, beta-pyridylcarbinol and control protocols. It increased to 960 +/- 71 mumol/l after the Intralipid infusion, fell to 246 +/- 17 mumol/l after the beta-pyridylcarbinol infusion, vs 600 +/- 48 mumol/l in the control. At the end of the glucose-insulin clamp the values were low in the 3 protocols: 263 +/- 17, 233 +/- 19 and 204 +/- 14 mumol/l. Intralipid infusion prior to the clamp protocol induced a suppression of both insulin-mediated glucose uptake (4.91 +/- 0.46 (Intralipid) vs 6.83 +/- 0.63 mg.kg-1.min-1 (saline)) and storage (1.61 +/- 0.34 vs 2.99 +/- 0.53 mg.kg-1.min-1) while beta-pyridylcarbinol infusion induced an increased insulin-mediated glucose uptake (8.58 +/- 0.37 mg.kg-1.min-1) and in glucose storage (4.29 +/- 0.31 mg.kg-1.min-1) (p less than 0.5 vs Intralipid). These changes occurred even though FFA plasma concentrations were similar in the 3 experimental conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗