PubMed Health⌕ Search

Biomedical subjects

T J Merimee

Publications and source records attributed to T J Merimee.

At least 73 records · Page 4Linked to original sources

Increased insulin binding by lymphocyte receptors induced by beta-OH butyrate.

The serum concentration of ketones increases in both fasting and diabetic ketoacidosis. Whether ketones alter, independent of changes in pH, in number and affinity of insulin receptors is not known. The binding of insulin 125I by 24 X 10(6)IM-9 lymphocyte cells was examined in both the presence and absence of 8 mM beta-OH butyrate. Studies were conducted at multiple concentrations of insulin. A consistent increase of insulin binding was induced by beta-OH butyrate. The mean maximum increase of insulin binding was 35%, which achieved significance at the 1% level.

Acidosis↗

Clinical and pathological studies in a growth hormone-deficient dwarf.

Postmortem studies were performed in one of three closely related dwarfs. Repeated arginine infusions and insulin tolerance tests never resulted in plasma levels of human growth hormone (HGH) greater than 2.0 ng/ml in any of these three dwarfs. However, pituitary somatotropes in the autopsied subject were well granulated and were reduced in number to 20% of normal. In the absence of a second defect, there should have been substantially higher HGH levels in plasma after provocative stimulation. The clinical and pathological data appear most compatible with (a) deficiency of growth hormone releasing factor, or (b) insensitivity of somatotropes to this material. It seems reasonable to postulate that a major group of dwarfs clinically simulating HGH deficiency can be explained by one of these mechanisms rather than by an absolute deficiency of HGH.

Adult↗

Metabolic studies in the African pygmy.

Major metabolic effects of human growth hormone (HGH) were assessed in the African Babinga pygmy. Plasma free fatty acid (FFA) and glucose concentrations were measured in pygmies, HGH-deficient dwarfs, Bantu tribesmen, and Caucasian controls after each received 4 mg of HGH intravenously over a 20 min period. Pygmies had an early decrease of plasma FFA and glucose concentration, but did not exhibit a later lipolytic response. In neighboring Bantu tribesmen, American controls, and HGH-deficient dwarfs, both the early and late responses to intravenous HGH were present. The failure of plasma FFA concentration to increase in the pygmy after intravenous HGH was not due to a generalized defect in lipolysis since a normal lipolytic response was obtained with epinephrine (2 mug/min for 20 min).Pygmies, like HGH-deficient dwarfs, had significantly reduced insulin responses to both oral glucose and arginine. Insulin secretion was significantly reduced when compared with either Bantu tribesmen or American controls and was not altered by 2 wk of a high carbohydrate/high protein diet. HGH treatment in pygmies (5 mg b.i.d. for 5 days) failed to augment either glucose or arginine-induced insulin secretion. Glucagon consistently caused normal insulin secretion in HGH-deficient dwarfs and was, likewise, effective in each pygmy studied. In two offspring from different pygmy mothers and Bantu fathers, insulin responses to glucose were initially normal and increased in a normal manner after HGH treatment. In previous studies, HGH failed to reduce serum urea nitrogen concentration in pygmies. Sulfation factor was found to be normal. A consideration of the data in toto is consistent with a hypothesis that the metabolic findings in the pygmy may result from partial nonresponsiveness to either HGH or to a factor generated by HGH. This defect is not transmitted as either an autosomal or sex-linked dominant trait.

Arginine↗