A. I. Vinik

Insulin secretion and pancreatic exocrine function in patients with chronic pancreatitis

SummaryThe relationship between insulin responses to oral glucose and pancreatic exocrine function were examined in 15 patients with chronic pancreatitis. Good correlations were found between the insulin responses and exocrine pancreatic function measured as the concentrations of pancreatic enzymes in duodenal juice after intravenous cholecystokinin-pancreazymin (CCK-PZ). There appears to be a roughly parallel loss of endocrine and exocrine function in the course of chronic pancreatitis.

Liver glycogen after portacaval shunt in rats.

Abstract Theories to explain the metabolic effects of portacaval shunt (PCS) have frequently failed to take into account the sequelae of PCS-induced anorexia. In this study PCS rats, followed up to 42 days postoperatively, had a lower food intake than ad libitum-fed (ALC) controls and also lost 10% body wt compared to a 20% gain of ALC rats. Liver weight was significantly reduced in PCS rats compared to ALC rats, pair-fed sham-operated (S) and pair-fed normal control (PFC) rats. However, liver glycogen was equally reduced in all animals with reduced food intake (PCS, S, and PFC rats) compared to ALC rats. Plasma glucose was significantly lower in PCS rats and PCS rats had markedly elevated plasma glucagon and lower plasma insulin concentrations than ALC rats, with the result that they had a low insulin: glucagon molar ratio of 1.3:1 compared to 10.2:1 in the ALC rats. The pair-fed control groups had intermediate I:G ratios and plasma glucose concentrations, thus an inverse relationship between mean plasma glucose and mean I:G ratio for each group was found, suggesting that the blood glucose concentration was the primary event determining the I:G ratio for each group. These controlled experiments indicate that hepatic atrophy after PCS appears to be directly related to the shunting of portal blood away from the liver, while reduced liver glycogen is related to decreased food intake. Reduction in total body weight, relative hypoglycemia, and elevated I:G ratios appear to be due to a combination of factors.

Studies on Raised Free Fatty Acids in Hyperthyroidism

In thyrotoxicosis the plasma free fatty acid levels are high before, suppress normally during, and rebound excessively 4–5 hours after an oral glucose load. The abnormal responses bear no relation to the plasma glucose, insulin and cortisol levels, and apparently effective blockade of 11- β -hydroxylation as well as α and β adrenergic receptor sites, effect no changes. Plasma growth hormone is not elevated, though glucose induced suppression is poor. Free fatty acid values return to normal on restoration of euthyroidism but alter after readministration of triiodothyronine (T3) to treated thyrotoxic as well as normal subjects. Growth hormone suppressibility likewise returns with euthyroidism and alters after T3 treatment in thyrotoxics, but these latter changes do not achieve statistical significance and are not reproduced in T3 treated normal controls. Although these results may be interpreted as in vivo evidence of a possible direct stimulatory effect of tri-iodothyronine or thyroxine on lipolysis in hyperthyroidism, the possibility exists that impaired suppression of growth hormone plays a role.