Insulin action and non-esterified fatty acids. The European Group for the Study of Insulin Resistance (EGIR).
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Adolescent↗
Biomedical subjects
A Golay
Publications and source records attributed to A Golay.
The role of dietary fat in obesity.
EPIDEMIOLOGY: Epidemiological evidence suggests that a high-fat diet promotes the development of obesity and that there is a direct relationship between the amount of dietary fat and the degree of obesity. The importance of this relationship has been shown in black prepubescent females, who consumed more calories as fat than white females. Moreover, black adult females are heavier and have significant higher cardiovascular disease mortality rates than white females. THE INFLUENCE OF DIETARY FAT ON FOOD INTAKE: An overview of animal studies had indicated that high-fat diets induce greater food intake and weight gain than high-carbohydrate diets. Several factors such as caloric density, satiety properties and post-absorbtive processing can contribute to this different response to high-fat diets. Accordingly, the satiating effects after meals with a high fat:carbohydrate ratio is less than for meals with a lower ratio. Some authors have reported that the most important variable influencing meal size is not the level of hunger but the nutrient content of the range of foods consumed. Thus dietary fat has a weak effect on satiety and we suggest that periodic exposure to a high-fat meal, particularly when hunger is high, may be sufficient to lead to overconsumption of energy as fat in obese patients. DIETARY FAT AND FAT BALANCE: Energy balance is well correlated with fat balance in lean controls, whereas there is no correlation with either carbohydrate or protein balances. Several authors have shown that carbohydrate and protein storage is closely regulated by adjusting oxidation to intake, whereas fat is almost exclusively used or stored in response to day-to-day fluctuations in energy balance. The positive relationship between fat intake and lipid oxidation seen in lean controls appears not to be present in obese patients. On high-fat diets, post-obese women failed to increase the ratio of fat to carbohydrate oxidation appropriately. Increasing dietary fat results in preferential fat storage in post-obese women, impaired suppression of carbohydrate and reduction of 24h energy expenditure. CONCLUSIONS: Dietary fat induces overconsumption and weight gain through its low satiety properties and high caloric density. Obese and post-obese subjects do not appear to adapt to dietary fat, and therefore fat storage is increased.
Adult↗
[Nutritional recommendations for diabetic patients: adaptation of the recommendations defined by the Diabetes and Nutrition Study Group of EASD].
Nutritional recommendations for diabetics are nowadays more flexible and better adapted to the individual patient. They resemble those offered to the public at large. Caloric intake is determined by body size and weight as well as physical activity. Approximately 60% of the energy should be consumed in the form of carbohydrates and monounsaturated fatty acids. The proportion of fatty acids and carbohydrates is fixed according to the individual nutritional habits. The intake of saturated and polyunsaturated fatty acids should be restricted. Meals and carbohydrates should be distributed over the day as three main meals with two to three snacks in between. Recommendations should always be adapted to the practical possibilities of the individual and to his particular metabolic situation.
Diabetes Mellitus↗
[Diet treatment of obesity--weight-loss stage and weight-maintenance stage].
Dietetic treatment of obesity occurs in two phases one of weight reduction and one of stabilisation of the reduced weight. Results of the first phase are marked mainly by reduction of calories (quantitative aspect) and not by the carbohydrate or fat content of the diet (qualitative aspect). This improves assessment of individual nutritional preferences and sustains the patients motivation longer. Current recommendations propose less restrictive diets, i.e. 500 Kcal less than the daily allowance. In the second phase of stabilisation a diet rich in complete carbohydrates (> 50 of daily calories) and poor in lipids (< 30%) regulates metabolism, appetite sencurion of saturation and thermogenesis favorably. Such a diet seems to permit a prolonged stabilisation of weight, an important criterion for successful treatment of obesity. A diet rich in carbohydrates and poor in lipids symbolized by a nutritional pyramid is at the same time the basis for actual recommendations for the entire population.
Diet, Reducing↗
[Diet and dyslipidemia].
In this article recommendations for dyslipidemias are illustrated by practical dietary recommendations for an individual patient with combined hyperlipidemia. Recommendations in hypercholesterolemia above all consist in the replacement of saturated by unsaturated forty acids thus reducing automatically cholesterol, too. In hypertriglyceridemias reduction of body weight should often be combined with quantitative control of alcohol and simple carbohydrates. A list of foods to be chosen or to be avoided is provided.
Dietary Fats↗
Risk factors associated with contrast sensitivity loss in diabetic patients.
BACKGROUND: Psychophysical tests in patients with diabetes mellitus reveal deficits of central vision before the development of overt retinopathy. We evaluated the contrast sensitivity thresholds in 30 patients with type II diabetes mellitus and without retinopathy, taking into account the crystalline lens density. Risk factors for contrast sensitivity deficits were investigated. METHODS: Contrast sensitivity was compared in 30 aretinopathic diabetic patients and age-matched controls. Contrast thresholds were determined for stationary gratings at three spatial frequencies (6, 15, and 27 cycles/deg) and for mesopic (5 cd/m2) and low photopic (85 cd/m2) vision. Lens density was measured using a IntraOptics opacity lensmeter. RESULTS: Significant contrast sensitivity losses at all three spatial frequencies were observed in low photopic and mesopic vision in diabetic patients. The optical density of the lens in the diabetic group did not differ from that in the controls. Contrast sensitivity deficits were positively correlated with patient's age, systolic blood pressure and nephropathy at all three spatial frequencies. No relationship between cardiovascular autonomic neuropathy and contrast sensitivity defects was observed. CONCLUSIONS: These data suggest that contrast sensitivity deficits in diabetic patients without retinopathy are not solely explained by a diabetes-induced increases in lens optical density. Abnormalities of the retina or its neural connections occurring before the onset of clinically detectable retinopathy may be involved. Risk factors for these deficits are advanced age, high systolic blood pressure, and nephropathy.
Adult↗
Similar weight loss with low- or high-carbohydrate diets.
The goal of this study was to evaluate the effect of diets that were equally low in energy but widely different in relative amounts of fat and carbohydrate on body weight during a 6-wk period of hospitalization. Consequently, 43 adult, obese persons were randomly assigned to receive diets containing 4.2 MJ/d (1000 kcal/d) composed of either 32% protein, 15% carbohydrate, and 53% fat, or 29% protein, 45% carbohydrate, and 26% fat. There was no significant difference in the amount of weight loss in response to diets containing either 15% (8.9 +/- 0.6 kg) or 45% (7.5 +/- 0.5 kg) carbohydrate. Furthermore, significant decreases in total body fat and waist-to-hip circumference were seen in both groups, and the magnitude of the changes did not vary as a function of diet composition. Fasting plasma glucose, insulin, cholesterol, and triacylglycerol concentrations decreased significantly in patients eating low-energy diets that contained 15% carbohydrate, but neither plasma insulin nor triacylglycerol concentrations fell significantly in response to the higher-carbohydrate diet. The results of this study showed that it was energy intake, not nutrient composition, that determined weight loss in response to low-energy diets over a short time period.
Adipose Tissue↗
Weight-loss with low or high carbohydrate diet?
OBJECTIVE: With obesity being recognized as an important cardiovascular risk factor, it is important to determine the optimal hypocaloric diet for decreasing that risk. The goal of this study was to compare the effects of two hypocaloric diets of similar caloric value, but differing in carbohydrate content (25% and 45%). SUBJECTS: Sixty-eight out-patients were followed for 12 w. DESIGN: The patients were assigned to one of two groups that received either a low (25% CHO, n = 31) or a high (45% CHO, n = 37) carbohydrate hypocaloric diet (5.0 MJ/d, 1200 Kcal/d). RESULTS: After 12 w, the mean weight loss was similar and did not differ significantly between the two groups: 10.2 +/- 0.7 kg (25% CHO) and 8.6 +/- 0.8 kg (45% CHO). Furthermore, loss of adipose tissue was similar, 8.1 +/- 0.5 kg (25% CHO) and 7.1 +/- 0.7 kg (45% CHO). Despite a high protein intake (1.4 g/kg/ideal body weight) there was loss of lean body mass: 2.2 +/- 0.4 kg (25% CHO) and 1.4 +/- 0.3 kg (45% CHO). The waist/hip ratio diminished significantly (P < 0.001) and identically in both groups. The fasting blood glucose (even though normal, along with cholesterol and triglyceride concentrations, were significantly decreased after weight loss. The fasting blood insulin which was mildly elevated before weight loss decreased more markedly with the 25% CHO diet compared to the 45% CHO diet (P < 0.003). The glucose/insulin ratio improved significantly (P < 0.05) after weight loss with both diets (0.17 +/- 0.04 mmol/mU (25% CHO) vs 0.10 +/- 0.03 mmol/mU (45% CHO). CONCLUSIONS: Neither diet offered a significant advantage when comparing weight loss or other, metabolic parameters over a 12 w period. However, considering the greater improvement of fasting blood insulin, the glucose/insulin ratio and blood triglyceride, the low carbohydrate diet (25%) could be more favourable in the long-term. The improvement of fasting blood insulin could be explained by the differences in monounsaturated fat composition in the low carbohydrate diet.
Adipose Tissue↗
The insulin-sparing effect of metformin in insulin-treated diabetic patients.
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Blood Glucose↗
Effect of lipid oxidation on the regulation of glucose utilization in obese patients.
The effect of changes in lipid oxidation on glucose utilization (storage and oxidation) was studied in seven nondiabetic obese patients. They participated in three protocols in which: (1) Intralipid (to raise plasma FFA concentrations), (2) beta-pyridylcarbinol [a precursor of nicotinic acid, to lower plasma free fatty acids (FFA) concentrations], or (3) isotonic saline were infused over 2 h. Thereafter, these infusions were discontinued, and a 2-h euglycemic, hyperinsulinemic clamp was performed to measure glucose uptake. All studies were carried out in combination with indirect calorimetry to measure oxidative and nonoxidative glucose disposal (glucose storage). The high plasma FFA concentrations (1024 +/- 57 mumol/l) and lipid oxidation rates (1.1 +/- 0.1 mg/kg.min) found at the end of the Intralipid infusion and the low plasma FFA concentrations (264 +/- 26 mumol/l) and lipid oxidation rates (0.7 +/- 0.1 mg/kg.min) found at the end of the beta-pyridylcarbinol infusions resulted in significantly different rates of total and nonoxidative glucose disposal during the insulin clamp. The values were 2.6 +/- 0.6 mg/kg.min after Intralipid and 4.1 +/- 1.0 mg/kg.min after beta-pyridylcarbinol for total glucose disposal, and 0.4 +/- 0.4 and 1.6 +/- 0.8, respectively for nonoxidative glucose disposal. In conclusion, these observations show that changes in lipid oxidation rates preceding a glucose load influence glucose disposal and glycogen storage in obese subjects.
Adult↗
Regulation of nutrient metabolism and energy expenditure.
The requisites for energy expenditure are covered mainly by two major substrates, glucose and free fatty acids (FFA). Their regulation and metabolism differ. After carbohydrate ingestion, glucose is rapidly oxidized or stored in muscles and liver. There is a constant alternance between glucose storage as glycogen after meals and glycogen mobilization in the postabsorptive state when plasma glucose has returned to the basal state. Impairment of this alternance, in particular when glycogen stores are not being used, may lead to glucose intolerance and insulin resistance. Ingestion of lipids is not followed by an immediate increase in lipid oxidation, but FFA are stored as triglycerides in different tissues. Lipolysis occurs in the fasting state from tissue triglycerides and favors lipid oxidation. Lipid oxidation is typically increased in obesity. The preferential use of FFA from triglyceride stores for energy expenditure in obesity is responsible for the decrease in glucose mobilization from glycogen stores. This leads to a negative feedback of muscle and liver glycogen on glycogen synthase activity and consequently on glucose storage. It results in glucose intolerance after carbohydrate ingestion. Diabetes develops in obesity, usually after a long period of glucose intolerance, when glycemia does not return to the basal state. In obesity, glucose intolerance and insulin resistance can be prevented, or if already existing, can be decreased by stimulating glycogen mobilization by exercise, thermogenesis-stimulating drugs, and weight loss, which reduces fat stores and decreases lipid oxidation.
Diabetes Mellitus, Type 2↗
Insulin sensitivity in obese hypertensive dyslipidemic patients treated with enalapril or atenolol.
We evaluated the effects of enalapril [angiotensin converting enzyme (ACE) inhibitor] in comparison with atenolol (beta-blocker) on insulin sensitivity and serum lipoprotein concentration in obese hypertensive dyslipidemic patients. Twenty-eight hypertensive [mean blood pressure (MAP) 152 +/- 3/103 +/- 1 mm Hgl], obese [mean body mass index (BMI) 30 + 1 kg/m2A], dyslipidemic [total triglycerides 2.0 +/- 0.2 mM and/or high density lipoprotein (HDL) cholesterol 1.1 +/- 0.1 mM and low density lipoprotein (LDL) cholesterol 4.5 +/- 0.2 mM] outpatients were randomized in two groups receiving enalapril or atenolol for 12 weeks, in an investigator-blinded, parallel, comparative two-center trial. Insulin sensitivity was assessed by a modified insulin suppression test. Blood pressure (BP), insulin sensitivity, and serum lipoprotein concentrations were compared before and after each treatment and between the two treated groups. BP decreased significantly and comparably during enalapril and atenolol treatment (p < or = 0.01). The sensitivity to insulin improved by 15% (p = 0.03) in the enalapril group and worsened by 17% (p < or = 0.01) in the atenolol group. Serum lipoprotein concentrations were not modified by any treatment. The improvement in insulin sensitivity caused by enalapril treatment appears to be an advantage as compared with atenolol treatment in hypertensive obese and dyslipidemic patients, whereas the BP-lowering efficacy of the two drugs is similar. Because this effect has been reported with other ACE inhibitors, it appears to be characteristic of the entire class of ACE inhibitors.
Adrenergic beta-Antagonists↗
Cardiovascular autonomic neuropathy in diabetic patients with macular oedema.
We performed a case-control study to investigate the determinants of macular oedema in patients with diabetes mellitus. Patients with macular oedema (n = 20) were selected for study, together with a random sample of subjects without macular oedema (controls, n = 21). Both groups were similar for sex, type of diabetes, treatment and glycaemic control. Patients with maculopathy had higher systolic and diastolic blood pressure than controls (P < 0.006 and P < 0.03, respectively). Impaired renal function was proportionally higher in patients with maculopathy than in controls (60% vs 47%). Vibratory perception was more impaired in the maculopathy group than the control group (P < 0.02), and maculopathy was associated with the presence of cardiovascular autonomic neuropathy. R-R variation and the brake index were significantly lower in patients than control subjects (P < 0.01 for both). Moreover, the group with maculopathy had a greater fall in systolic blood pressure after standing than did the control group (P < 0.0001). Autonomic neuropathy may be associated with the development of maculopathy and retinopathy, although additional evidence is required to confirm this association. Conditions associated with high blood pressure may accelerate progression and aggravate maculopathy.
Adult↗
[From obesity to diabetes].
The frequent development of Type 2 diabetes in the obese suggests a relationship between obesity and diabetes. This study presents evidence for a continuum form obesity to diabetes via glucose intolerance and hyperinsulinemic diabetes. The defect which seems to be at the origin of this development resides in the increase in lipid oxidation already present in the early stages of obesity. It reflects the increased utilisation of fatty acids for energy purpose in the obese, at the expenses of glucose. In non-diabetic obese subjects, insulin resistance can be demonstrated by the inhibition of glucose storage during a euglycemic, hyperinsulinemic, clamp. This defect in glucose storage is not observed during a oral glucose tolerance test (OGTT), as it is compensated by hyperinsulinemia and hyperglycemia during glucose tolerance. Glucose tolerance appears with the inhibition of glucose oxidation by the augmented lipid oxidation. This decreased glucose utilization causes a slowdown of the utilization of glycogen stores which leads, as a consequence, to the inhibition of glycogen synthase by its product, glycogen. Diabetes appears when the increase in glycemia and insulinemia does not compensate any more for the inhibition of glucose storage. The rise in basal glycemia simultaneously with the fall in glucose storage corresponds to the transition to diabetes. The decreased glucose mobilization together with the inhibition of glycogen phosphorylase are such in the diabetic patient that glycogen stores tend to remain full and glycogen synthase is inhibited by negative feedback. The retrograde inhibition of glycogen stores on glycogen synthase activity brings up incapacity to store glucose and leads to a rise in glycemia. Finally, the evolution of obesity to diabetes leads to a decrease in insulin secretion with increase in hepatic glucose production through gluconeogenesis and decreased capacity to store glucose. Therapeutic implications are discussed in this review.
Adult↗
The effect of the gastrointestinal lipase inhibitor, orlistat, on serum lipids and lipoproteins in patients with primary hyperlipidaemia.
The effect of orlistat, a nonabsorbed inhibitor of gastric and pancreatic lipases, was examined in patients with primary hyperlipidaemia (serum cholesterol > or = 6.2 mmol.l-1 and triglycerides < or = 5.0 mmol.l-1) not responsive to dietary change alone. In a multicentre, randomised, double-blind study, 103 men and 70 women received 30, 90, 180, or 360 mg or orlistat or placebo for 8 weeks. Total and low-density lipoprotein cholesterol levels were reduced by 4% and 5% with 30 mg orlistat, by 7% and 8% with 90 mg orlistat, by 7% and 7% with 180 mg orlistat and by 11% and 10% with 360 mg orlistat compared to placebo. High density lipoprotein cholesterol levels significantly decreased in the 360 mg orlistat group. Triglyceride levels significantly increased in the placebo group but not in the drug groups. Body weight decreased by 1.2 kg with 360 mg orlistat, despite a weight maintenance diet. Decreases in vitamin E and D levels occurred, although both vitamins remained within the normal range. Adverse effects from the gastrointestinal tract were frequent, but led to discontinuation of therapy in only seven patients. Orlistat is a new therapeutic drug for the treatment of hyperlipidaemia that may be particularly useful among overweight patients. Its potential place in therapy will await long-term studies. Vitamin supplementation should be considered during treatment.
Adult↗
Effect of a novel beta-adrenoceptor agonist (Ro 40-2148) on resting energy expenditure in obese women.
The aim of this single-blind, placebo-controlled study was to investigate the effects of the new beta-adrenergic compound Ro 40-2148 on resting energy expenditure (REE) at rest and after an oral glucose load in non-diabetic obese women before and after two weeks of treatment. After one week of placebo administration and after an overnight fast and one hour rest, REE and glucose and lipid oxidation rates were measured by indirect calorimetry (hood system) before and for 6 h after a single dose of placebo solution. A 75 g oral glucose tolerance test (OGTT) was performed during this period starting 90 min after the placebo administration. During the following two weeks, using a randomization design, six patients received Ro 40-2148 at a dose of 400 mg diluted in 100 ml water twice a day (i.e. 800 mg per day), while six others continued with the placebo administration. The same tests and measurements were repeated after two weeks, except for the treatment group which received the drug instead of the placebo. The 14-day period of drug administration did not increase REE measured in post-absorptive conditions. Similarly, there was no acute effect on REE of a 400 mg dose of Ro 40-2148. In contrast, glucose-induced thermogenesis was significantly increased after two weeks in the treatment group (means +/- s.e.m.: 3.7 +/- 1.3%, P = 0.047), while no change was observed in the placebo group (-0.8 +/- 0.7%, not significant). Since there was no significant change in the respiratory quotient, the increase in energy expenditure observed in the treatment group was due to stimulation of both lipid and glucose oxidation. The drug induced no variations in heart rate, blood pressure, axillary temperature or in plasma glucose, insulin and free fatty acid levels. In conclusion, this study shows that Ro 40-2148 activates glucose-induced thermogenesis in obese non-diabetic patients.
Adrenergic beta-Agonists↗
[Policy on diabetes nutrition 1994].
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Blood Glucose↗