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Biomedical subjects

D Porte

Publications and source records attributed to D Porte.

At least 235 records · Page 13Linked to original sources
PubMed1970

Abnormal lipid composition of chylomicrons in broad-beta disease (type 3hyperlipoproteinemia).

Chylomicron (primary particles) were detected by polyvinylpyrollidone (PVP) flocculation in plasma collected after an overnight fast from eight hyperlipemic subjects with broad-beta disease (type III hyperlipoproteinemia). The composition of these chylomicrons was abnormal: relatively poor in triglyceride and rich in cholesterol, giving rise to a triglyceride/cholesterol ratio of < 3.0 in all cases, uniformly below the ratio in chylomicrons from eight fasting subjects with mixed lipemia. By contrast, at the peak of alimentary lipemia following an oral fat load (2 g/kg), chylomicrons from broad-beta subjects had normal, triglyceride-rich composition (triglyceride/cholesterol = 14.0) and resembled chylomicrons from subjects with mixed lipemia, endogenous lipemia, and familial hypercholesterolemia after similar fat loads. As the alimentary lipemia cleared, chylomicrons remaining in broad-beta subjects 14-24 hr after the fat load were again rich in cholesterol. However, a similar degree of cholesterol enrichment was observed in chylomicrons from the subjects with familial hypercholesterolemia, while only a minor increase in cholesterol was recorded in chylomicrons from subjects with mixed or endogenous lipemia. Parallel studies of changes in chylomicron composition during in vitro incubation of whole plasma and of S(f) > 400 with S(f) < 400 lipoproteins from subjects with the different forms of hyperlipoproteinemia revealed equal cholesterol enrichment of chylomicrons from a subject with mixed lipemia and from a subject with broad-beta disease in media of equivalent cholesterol content. These experiments suggested neither excessive avidity of chylomicrons for cholesterol uptake nor excessive influence of S(f) < 400 lipoproteins upon chylomicron composition in broad-beta disease.Thus, results in this study suggest that the cholesterol-rich chylomicrons observed in subjects with broad-beta disease after an overnight fast may originate in the intestine as particles of normal composition (chiefly dietary triglyceride) but assume a composition which is relatively rich in cholesterol through processes of lipolysis and cholesterol transfer among circulating lipoproteins which may not be unique to broad-beta disease.

Cholesterol↗
PubMed1970

Uniphasic insulin responses to secretin stimulation in man.

Secretin-stimulated insulin release was studied in normal subjects. In response to rapid intravenous injections (pulses) of secretin, insulin levels reached a peak between 2 and 5 min and returned to basal levels with 15 min. In contrast to large glucose pulses, increasing secretin pulses did not elicit sustained or prolonged insulin responses. In addition, insulin responses to a pulse and infusion were essentially identical with that of a pulse alone. Increasing secretin pulses given in 1 day were associated with decreasing insulin responses but not when the same pulses of secretin were given over a 2 day period. When time was the sole variable, insulin responses progressively decreased after identical 15-U secretin pulses given every 30 min, but were unchanged when the interval was 105 min. These observations indicate that secretin in contrast to glucose stimulates insulin release which is uniphasic. They suggest that release occurs only from a stored, readily available pool. This insulin pool appears to be relatively small and can be discharged faster than it refills.

Blood Glucose↗
PubMed1969

Insulin responses to glucose: evidence for a two pool system in man.

Four rapid glucose injections of 5 g each were administered to normal young adult subjects before, during, and after an infusion of glucose. After the first glucose pulse, insulin responses measured immunologically reached a peak between 3 and 5 min and rapidly returned to base line. A short glucose infusion of 300 mg/min decreased the rapid insulin response to a second glucose pulse (- 58%), but after a longer infusion (20 hr) the acute insulin response to a third pulse was restored to normal. Stopping the infusion was followed by return of glucose and insulin levels to prestudy base line within 1 hr, but a fourth glucose pulse was followed by a supernormal acute insulin response (+ 200%). Other observations during these studies showed that a short glucose infusion of either 100 mg/min or 300 mg/min produced a parallel rise in glucose and insulin, but continuation of the infusion for 20 hr was associated with a "paradoxical" fall in glucose and continued rise in insulin. These observations are considered incompatible with a simple linear model often used to describe the relation between plasma glucose and serum insulin. Instead, a two pool system-one for acute insulin release, and the other a time-dependent compartment for long term insulin responses-is suggested.

Adult↗