1,721,012 research outputs found
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
Residual B cell function and insulin sensitivity in type 1 (insulin-dependent) diabetes mellitus.
No full textProstaglandine e ipertensione arteriosa: ipotesi patogenetiche e prospettive terapeutiche
No full textInadeguatezza della misurazione dei livelli circolanti di insulina nella valutazione dell'attività secretoria beta-cellulare pancreatica.
No full textValutazione della presenza di neuropatia autonomica in diabetici asintomatici di tipo I e II.
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Decreased hepatic insulin extraction in subjects with mild glucose intolerance.
No full textThe fact that hyperinsulinemia occurs in simple obesity and mild glucose intolerance has been well established. Altered hepatic insulin extraction may influence the levels of circulating hormone. The simultaneous measurement of insulin and C-peptide concentrations in peripheral blood enables an in vivo estimation of hepatic insulin removal. To evaluate hepatic insulin extraction, insulin and C-peptide responses to oral glucose were studied in 176 obese and nonobese subjects with normal, impaired, or diabetic glucose tolerance. Insulin levels as well as insulin incremental areas in glucose intolerant subjects were significantly higher than in weight-matched controls. The levels of C-peptide as well as C-peptide incremental areas were only slightly enhanced in subjects with impaired glucose tolerance, whereas they were reduced in subjects with diabetic tolerance. The molar ratios of C-peptide to insulin, both in the fasting state and after ingestion of glucose, as well as the relationship between the incremental areas of the two peptides were used as measures of hepatic insulin extraction. They were significantly reduced in glucose intolerant subjects and, to a lesser extent, in nondiabetic obese subjects. These results indicate that peripheral hyperinsulinemia in subjects with simple obesity or impaired glucose tolerance is a result of both pancreatic hypersecretion and diminished hepatic insulin extraction. In subjects with a more severe degree of glucose intolerance, decreased hepatic insulin removal is the primary cause of hyperinsulinemia
Diminished pituitary responsiveness to growth hormone releasing factor in aging male rats
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