1,721,148 research outputs found
Inhibition of carbohydrate-induced hypertriglyceridemia by a disaccharidase inhibitor.
No full textThe ability of an inhibitor of intestinal alpha-glucosiadase activity to prevent sucrose-induced hypertriglyceridemia was studied in nonobese rats. The results indicated that plasma triglyceride levels were approximately twice as high in untreated rats, and the reduction in plasma triglyceride levels of drug-treated rats was associated with lowered very low density lipoprotein-triglyceride secretion rates and plasma insulin levels. Since these changes could be produced with an amount of glucosidase inhibitor which did not prevent normal rate of weight gain, the possibility arises that this approach may be useful in the treatment of various hypertriglyceridemic states in man. Finally, the observation that the fall in plasma TG concentration was associated with a fall in plasma insulin concentration provides further evidence for the existence of a causal relationship between the two variables
Insulin-resistance and associated risk factors for coronary heart disease as seen in families.
No full textRecent reports have shown that resistance to insulin-stimulated glucose uptake, increased plasma glucose and insulin response to oral glucose, and hypertriglyceridemia can be seen in first degree relatives of patients with type 2 diabetes. We have recently shown that very similar metabolic changes can be seen in hyperinsulinemic individuals who have either normal or impaired glucose tolerance (IGT). Given these data, we thought it would be of interest to compare the plasma glucose and insulin response to an oral glucose challenge, plasma lipid concentrations, and blood pressure in offspring of parents with IGT as compared to offspring of parents with normal glucose tolerance. Parents with IGT had higher plasma insulin and triglyceride levels and blood pressure than those with normal glucose tolerance. The two groups of offspring were young, non-obese and similar in terms of age, gender distribution and body mass index. Statistically significant increases in plasma insulin response to oral glucose and in systolic and diastolic blood pressure were present in the offspring of parents with IGT. Demonstration of similar abnormalities in plasma insulin response to glucose and blood pressure regulation in patients with IGT and in their offspring is consistent with the view that individual differences in insulin metabolism and blood pressure are modulated by genetic factors and that both may be related to variations in insulin-stimulated glucose uptake and/or plasma insulin concentration
Proprietà cardioprotettiva degli antidiabetici orlai e ruolo delle cellule progenitrici endoteliali e della lunghezza dei telomeri nel rischio cardiovascolare.
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Insulin release in hyperuricemic patients
No full textThe insulin response to oral glucose and to i.v tolbutamide was stuied in a group of hyperuricemic subjects and in a group of weight-matched controls. Glucose tolerance was impaired only in obese hyperuricemic subjects. Insulin response to oral glucose was enhanced in hyperuricemic subjects. Tolbutamide gave rise to a sharp increase in IRI levels already 2 min after the injection and this rise was significantly higher in hyperuricemic subjects than in controls. The same result was observed also after i.v. fructose. The interpretation of these data is not easy. Uric acid plasma level and obesity do not seem to be directly involved because an abnormal IRI response has been observed also after a rapid fall in uric acid plasma level after allopurinol treatment and is evident also in lean subjects. In our opinion the problem is more complex and must be considered from the point of view of a change involving carbohydrate as well as purine metabolism
Studies of the mechanism of fructose-induced hypertriglyceridemia in the rat
No full textCarbohydrate-induced hypertriglyceridemia is easily produced in the rat, and fructose has been shown to be particularly potent in this regard. In this study we have compared the effects of feeding rats diets high (66% of total calories) in fructose or glucose on various aspects of carbohydrate and lipid metabolism. The results confirmed previous observations that fructose (456 +/- 276 mg/dl) was more potent (p less than 0.001) in raising plasma TG concentration than was glucose (242 +/- 13 mg/dl), and indicated that the difference in magnitude of hypertriglyceridemia produced by the two carbohydrates was closely related to the ability of the test diets to increase VLDL-TG secretion (r = 0.85, p less than 0.001). Both glucose and fructose feeding led to comparable degrees of hyperinsulinemia, and plasma TG concentrations increased before hyperinsulinemia evolved in fructose-fed rats. Therefore, it was concluded that fructose can act directly on the liver to increase VLDL-TG secretion, and that fructose-induced hypertriglyceridemia can occur in the absence of hyperinsulinemia. On the other hand, the rise in plasma TG concentration produced by fructose was reduced dramatically in exercise-trained rats, and this was associated with a decrease in plasma insulin concentration. Based upon these observations, we suggest that fructose feeding produces hypertriglyceridemia by directly stimulating hepatic VLDL-TG secretion, as well as by producing insulin resistance and hyperinsulinemia, and that it is the combined effect of these two separate actions which accounts for the magnitude of fructose-induced hypertriglyceridemia
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