This study investigated the percentage of carbohydrate utilization than can be accounted for by glucose ingested during exercise performed after the ingestion of the potent lipolysis inhibitor Acipimox. Six healthy male volunteers exercised for 3 h on a treadmill at about 45% of their maximal oxygen uptake, 75 min after having ingested 250 mg of Acipimox. After 15-min adaptation to exercise, they ingested either glucose dissolved in water, 50 g at time 0 min and 25 g at time 60 and 120 min (glucose, G) or sweetened water (control, C). Naturally labelled [13C]glucose was used to follow the conversion of the ingested glucose to expired-air CO2. Acipimox inhibited lipolysis in a similar manner in both experimental conditions. This was reflected by an almost complete suppression of the exercise-induced increase in plasma free fatty acid and glycerol and by an almost constant rate of lipid oxidation. Total carbohydrate oxidation evaluated by indirect calorimetry, was similar in both experimental conditions [C, 182, (SEM 21); G, 194 (SEM 16) g.3 h-1], as was lipid oxidation [C, 57 (SEM 6); G, 61 (SEM 3) g.3 h-1]. Exogenous glucose oxidation during exercise G, calculated by the changes in 13C:12C ratio of expired air CO2, averaged 66 (SEM 5) g.3 h-1 (19% of the total energy requirement). Consequently, endogenous carbohydrate utilization was significantly smaller after glucose than after placebo ingestion: 128 (SEM 18) versus 182 (SEM 21) g.3 h-1, respectively (P < 0.05). Symptoms of intense fatigue and leg cramps observed with intake of sweet placebo were absent with glucose ingestion.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1994

Therapy for obesity--today and tomorrow.

Obesity poses a serious health hazard and its treatment is often disappointing. Besides conservative methods, the place of pharmacotherapy, very-low-calorie diets, and even, in selected cases, mechanical means or surgery can be considered. Effective drug treatment for obesity must reduce energy intake, or increase energy expenditure, or increase energy losses in faeces. All these possibilities have potential activities but also serious limitations. Current pharmacotherapy essentially uses anorectic drugs and the other approaches, although promising, are still under investigation. Of the anorectic compounds currently available, serotoninergic agents, like dexfenfluramine and fluoxetine, appear to have the most suitable pharmacological profile. Very-low-calorie diets could help in the short-term but should be associated with other approaches to increase the rate of long-term success. They must be well-balanced as macronutrients and micronutrients are concerned, be prescribed in well-selected patients under careful medical supervision, and not be followed longer than a few weeks. Surgery can provide palliation for severe obesity when all medical approaches have failed. It may consist in decreasing food intake (gastric procedures), affecting calorie absorption (intestinal shunting, biliopancreatic bypass), or removing localized excess fat (lipectomy, liposuction). Gastric reduction operations are safe and effective provided they are performed by experienced surgeons in well-selected patients. They can be considered now as the best option for a minority of patients with morbid and refractory obesity. Finally, in very selected patients, mechanical means (such as the waist cord) may also help losing weight and/or avoiding weight regain. Even if all these therapeutic approaches can be helpful, at least in some obese individuals, they also have important limitations so that prevention remains up to now the 'treatment' of choice for obesity.

Appetite Depressants↗

PubMed1994

The use of acarbose in the prevention and treatment of hypoglycaemia.

This paper reviews the use of acarbose in the prevention and treatment of hypoglycaemia. In diet- or sulfonylurea-treated patients, acarbose may reduce the incidence of late postprandial hypoglycaemia. In insulin-treated patients, acarbose treatment usually requires reduction of the insulin dose; one study has shown that 100 mg acarbose at night significantly reduces the incidence of mid-evening and nocturnal hypoglycaemia. Several studies have suggested acarbose to be a useful adjunct to the management of reactive hypoglycaemia in the non-diabetic patients. Long-term prospective studies are still needed to document this last indication of acarbose or other alpha-glycosidase inhibitors.

Acarbose↗

PubMed1994

Reduction of the acute bioavailability of metformin by the alpha-glucosidase inhibitor acarbose in normal man.

In a double-blind cross-over study, we investigated a possible influence of the alpha-glucosidase inhibitor acarbose on the bioavailability of the biguanide compound metformin. Each of the six healthy young male volunteers was randomly allocated during two consecutive 7 day periods to either acarbose (days 1-3: 3 x 50 mg day-1; days 4-7: 3 x 100 mg day-1) or placebo. At day 7 and 14 of the study, the overnight-fasted subjects ingested 1000 mg metformin with the first bite of a standardized breakfast (500 kcal; 60 g carbohydrates) and together with either placebo or 100 mg acarbose. Acarbose significantly (P < 0.05) reduced the meal-induced increase in blood glucose and plasma insulin levels. Acarbose induced a significant (P < 0.05) reduction in early (90, 120, 180 min) serum levels, peak concentrations (Cmax: 1.22 +/- 0.14 vs. 1.87 +/- 0.60 mg l-1) and area under the curve of metformin (AUC 0-540 min: 423 +/- 55 vs. 652 +/- 55 mg min l-1), but did not diminish its 24 h urinary excretion. In conclusion, acarbose significantly reduces the acute bioavailability of metformin in normal subjects.

Acarbose↗

PubMed1994

Abnormal temporal patterns of glucose tolerance in obesity: relationship to sleep-related growth hormone secretion and circadian cortisol rhythmicity.

To define the chronobiology of glucose tolerance and insulin secretion in obesity, nine obese men and nine lean men were studied during constant glucose infusion for 53 h, including 8 h of nocturnal sleep, 28 h of continuous wakefulness, and 8 h of daytime sleep. Blood samples were collected at 20-min intervals to assay glucose, insulin, C-peptide, cortisol, and GH. Sleep was polygraphically monitored. Abnormal temporal profiles of glucose regulation were observed during wakefulness and sleep in obese subjects. During daytime hours, the normal profile of glucose tolerance was reversed, as an improvement, rather than a deterioration, was observed from morning to late evening. This reversal of the daytime pattern appeared to be caused by a dual defect in glucose regulation during the previous night. Indeed, during early sleep, GH secretion was markedly reduced, and the nocturnal rises of glucose and insulin secretion were dampened. During late sleep, obese subjects failed to suppress insulin secretion and plasma glucose, resulting in high morning levels. Comparisons of metabolic and hormonal patterns during nocturnal and daytime sleep suggest that the failure to suppress insulin secretion in late sleep may reflect a relative insensitivity of the beta-cell to acute inhibitory effects of cortisol in addition to insulin resistance.

Adult↗