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E W Chideckel

Publications and source records attributed to E W Chideckel.

24 records · Page 2Linked to original sources
PubMed1977

Assessment of obesity in pigtailed monkeys (Macaca nemestrina).

Obesity was studied in a colony of 873 Macaca nemestrina to establish tools for epidemiologic studies, to examine a genetic form of obesity, to document age/sex relationships to obesity, and to compare metabolic profiles of obese and normal monkeys. Age/weight growth curves were analyzed to select the most obese monkeys and age- and sex-matched normal controls. Degree of adiposity was determined using tritiated water for estimation of lean body mass. Body weight, anterior trunk height, and abdominal and triceps skinfolds were measured. Fasting insulin, fasting free fatty acids, and glucose disappearance rate were determined. The results give evidence of similarities between macaque and human obestiy.

Age Factors↗
PubMed1975

Adaptation to fasting in baboon. II. Regulation of lipolysis early and late in fasting.

Regulation of lipolysis by the sympathetic nervous system, basal insulin, and glucagon was studied in fasted baboons. Beta-Adrenergic mechanisms were evaluated by blockade with propranolol after 24, 40, and 65 h of fasting. Inhibition of lipolysis decreased with increasing duration of fasting. Insulin concentrations were markedly reduced by propranolol at all stages of fasting, whereas glucose and glucagon concentrations were unchanged. The roles of insulin and glucagon were evaluated by a 2-h infusion of somatostatin after 18 and 65 h of fasting. At both times, insulin and glucagon concentrations were markedly reduced. At 18 h of fasting but not at 65 h, lipolysis doubled. At both times the plasma glucose concentration fell 15-30%. At 18 h, preventing the decrease in glucose with glucose infusion prevented the increase in lipolysis. These data suggest that a beta-adrenergic mechanism is largely responsible for regulation of lipolysis early in fasting and that insulin, glucagon, and beta-adrenergic mechanisms play no major part in the maintenance of the accelerated lipolysis later in fasting.

Animals↗
PubMed1975

Somatostatin blockade of acute and chronic stimuli of the endocrine pancreas and the consequences of this blockade on glucose homeostasis.

The nature and extent of somatostatin-induced inhibition of pancreatic endocrine secretion were studied by administration of a number of stimuli of either glucagon or insulin to over night fasted baboons with and without an infusion of linear somatostatin. The stimuli for acute-phase insulin release were intravenous pulses of glucose, tolbutamide, isoproterenol, and secretin. When given 15 min after the start of a somatostatin infusion, these agents were essentially unable to stimulate insulin secretion. Chronic insulin secretion was stimulated by infusions of either glucose or glucagon. Within 10 min of the start of a super-imposed infusion of somatostatin, insulin levels fell to less than 40 percent of prestimulus control and remained suppressed for the duration of the somatostatin infusion. Stimulation of glucagon secretion by insulin-induced hypoglycemia was also blocked by somatostatin. Plasma glucose decreased during somatostatin infusions except when superimposed upon an infusion of glucagon. Somatostatin had no effect on glucose production in a rat liver slice preparation. We conclude: (a) Somatostatin is a potent and so far universally effective inhibitor of both acute and chronic phases of stimulated insulin and glucagon secretion (b) The inhibitory effect is quickly reversible and the pattern of recovery of secretion is appropriate to prevailing signals; (c) Present evidence suggests that the effect of somatostatin on blood glucose is mediated through its effect on blood glucagon; (d) In the overnight-fasted baboon both in the basal state and 45 min into a 4-mg/kg-min glucose infusion, a somatostatin-induced fall in serum insulin levels appears to be unable to prevent a decrease in hepatic glucose production.

Animals↗
PubMedDate not supplied

Effect of caffeine on tone and intracellular Ca++ release in guinea-pig and human trachealis.

High concentrations of methylxanthines induce contraction in many smooth muscle types, but relax guinea-pig trachealis. We examined this discrepancy by studying the interaction of caffeine and spasmogens in the isolated guinea-pig trachealis. We extended our observations to the isolated human trachealis. In the guinea-pig trachealis, 25 mM but not 2.5 mM caffeine totally blocked any contractile effect of methacholine or histamine, but not of KCl, whose contractile effect relies on extracellular Ca++. The beta-adrenergic agent isoprenaline (10(-3)M) only partially blocked the spasmodic effect of methacholine and histamine. In the human trachealis, 25 mM but not 2.5 mM caffeine induced an initial contraction followed by a relaxation. After this latter relaxation, methacholine (10(-5) M) and histamine (10(-5) M) were without effect, while KCl caused a contraction. In the guinea-pig, a contractile effect of 25 mM but not 2.5 mM caffeine was uncovered by switching to a high K+, Ca(++)-free solution prior to adding the caffeine. The source of the Ca++ promoting the contraction thus must be intracellular stores. Accordingly, ryanodine, an inhibitor of Ca++ storage, blocked this contraction. Similarly histamine (10(-5) M) and methacholine (10(-5) M) in the Ca(++)-free solution induced a contraction. The histamine contraction was completely blocked by ryanodine, the methacholine contraction, 79% blocked. We conclude that caffeine appears to surpass the antispasmodic effects of beta-adrenergic stimulation, at least in part, by depleting intracellular stores of Ca++.

Animals↗