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Biomedical subjects

D Elahi

Publications and source records attributed to D Elahi.

104 records · Page 6Linked to original sources
PubMed1982

Interaction of arginine and gastric inhibitory polypeptide on insulin release in man.

The interrelations of the insulin secretagogues, glucose, arginine (Arg), and gastric inhibitory polypeptide (GIP) were quantified in six normal young men in five sets of experiments with the hyperglycemic clamp technique (125 mg/dl above basal glucose levels for 2 h). After 60 min of intravenous glucose alone, one of the following was added: A) oral glucose (OG) (40 g/m2); B) 15 g.m-2.h-1 Arg infusion; C) 15 g.m-2.h-2 Arg infusion and OG; D) 7.5 g.m-2.h-1 Arg; E) 7.5 g.m-2.h-1 Arg and OG. The clearance rate of Arg was similar for B, C, D, and E. In all experiments, plasma GIP levels were unchanged from the basal level during the 1st h. The increases in plasma GIP levels in experiments C and E were similar to the increase when OG alone was ingested (A). When the stimulatory effect of the secretagogue(s) alone on insulin (IRI) is computed, the increase due to OG (A) and to 7.5 g.m-2.h-1 Arg (D) were similar and additive (A + D approximately equal to E). However, the stimulatory effect of 15 g.m-2.h-1 Arg + OG (C) on IRI was not significantly greater than 15 g.m-2.h-1 alone (B). The 15 and 7.5 g.m-2.h-1 Arg infusion produced different patterns of insulin and glucagon secretions. At the lower dose, the response of both hormones to Arg decreased with time. Arg and GIP act through a similar and possibly common mechanism on the beta-cell. However, only Arg was found to be alpha-cytotropic. GIP does not appear to influence the metabolic clearance of Arg. The dose-response relationships to Arg of the beta- and alpha-cell appear similar.

Adult↗
PubMed1981

Effects of age on control of lipolysis during fasting.

Loss of body weight, girth, epididymal fat pad weight, and adipocyte size were examined in male, virgin, Wistar rats aged 2, 6, 12 and 22-24 months during 5 days of fasting. Relative reductions in all four parameters were greatest in the 2-month-old animals, with little differences among the older three age groups. In contrast, absolute weight loss was greatest in 12, and 24-month-old rats. Body weights were also greatest in these two groups. Plasma epinephrine and norepinephrine increased to the same levels in all 4 groups during the fast. Similarly, insulin decreased to the same levels in all groups although the oldest rats already exhibited low levels prior to fasting. Thus, possible age differences in the lipolytic response to fasting do not appear due to age-related differences in important lipolytic (catecholamine) and antilipolytic (insulin) hormone levels. Possible age-related differences in lipolytic response to fasting may instead reflect changes in other hormones which regulate lipolysis, or an altered sensitivity of adipocytes to such hormones.

Aging↗
PubMed1981

Discrepant performance on oral and intravenous glucose tolerance tests: the role of gastric inhibitory polypeptide.

Analysis of a large study population revealed a group of eight healthy men whose tolerance to oral glucose was markedly greater than their tolerance to iv glucose (disparate group). The physiological basis of the anomalous performance was investigated using a variation of the hyperglycemic glucose clamp technique. This technique allows separation of the effects of hyperglycemia and intestinal insulinotropic factors on B-cell response. The eight subjects with disparate tolerance tests were compared to eight healthy control subjects whose tolerances on the two tests were very similar. The disparate performers showed 1) higher basal circulating gastric inhibitory polypeptide (GIP) levels, 2) lower immunoreactive insulin (IRI) responses to hyperglycemia (iv glucose alone), 3) enhanced GIP response to oral glucose, and 4) enhanced IRI response to oral glucose. These results may be interpreted as indicating a role for GIP in the improved tolerance for oral glucose, although other unknown gastrointestinal hormones could theoretically also be involved. Enhanced release of GIP after oral glucose may compensate for the reduced IRI release in response to hyperglycemia. The mechanism underlying the enhanced GIP response in these studies remains to be explored. It will be of interest to follow these subjects to see whether their anomalous gut beta-cell balance has any long term pathogenetic implications.

Administration, Oral↗
PubMed1978

Oral glucose augmentation of insulin secretion. Interactions of gastric inhibitory polypeptide with ambient glucose and insulin levels.

Gastric inhibitory polypeptide, or GIP, has been postulated as the major enteric hormonal mediator of insulin release. The release of immuno-reactive GIP (IR-GIP) after oral glucose and its role in insulin release was studied in normal men by the glucose clamp technique. In 24 subjects studied with the hyperglycemic clamp, blood glucose was maintained at 125 mg/dl above basal for 2 h via a primed-continuous IV glucose infusion coupled to a servo-controlled negative feedback system. 40 g glucose per m(2) surface area was ingested at 60 min, and the blood glucose was maintained at the steady-state hyperglycemic level. Plasma IR-GIP and insulin (IRI) levels were measured throughout the 2-h period. IR-GIP levels changed little when IV glucose alone was given; the mean basal value was 305+/-34 (SEM) pg/ml. After oral glucose, IR-GIP levels began to rise within 10 min and reached a peak within 40 min of 752+/-105 pg/ml. Plasma IRI responded initially to the square wave of hyperglycemia in the typical biphasic pattern. After oral glucose, plasma IRI levels rose strikingly above the elevated levels produced by hyperglycemia alone, reaching a peak of 170+/-15 muU/ml within 45 min. The time course of the rise in IR-GIP and IRI was nearly identical. To assess whether the maintenance of euglycemia would affect this process, the euglycemic clamp was employed in 11 subjects to maintain basal blood glucose levels during a similar 2-h study. A primed-continuous insulin infusion, with a constant rate of 120 mU/m(2) per min was given together with a servo-controlled glucose infusion. This resulted in hyper-insulinemia of approximately 300 muU/ml. Glucose was ingested by six subjects at 60 min. Plasma IR-GIP responded to oral glucose similarly to the effect seen in the hyperglycemic studies. No increase in endogenous insulin release was seen despite the increase in IR-GIP when euglycemia was maintained. However, in five of seven subjects given insulin whose blood glucose concentration rose by 20 mg/dl or more after oral glucose, there was an increase in plasma insulin concentration associated with the elevation in IR-GIP. Thus, the effect of glucose-released IR-GIP on insulin secretion is dependent upon the presence of some degree of hyper-glycemia and is not inhibited in the presence of marked hyperinsulinemia.

Adolescent↗
PubMed1977

Glucose kinetics in dogs following a lethal dose of endotoxin.

The effects of a lethal dose of Escherichia coli endotoxin on the glucose kinetics and cardiovascular responses of conscious dogs were studied. The plasma glucose level fell steadily after endotoxin administration to severely hypoglycemic levels preterminally. The fall in plasma glucose appeared to be due primarily to an increased tissue uptake in the early phase, whereas decreased hepatic glucose output also contributed in the later, preterminal phases.

Animals↗
PubMed1977

Glucose and lactate kinetics after endotoxin administration in dogs.

We studied the effects of E. coli endotoxin on the glucose and lactate kinetics in dogs by means of the primed constant infusion of [6(-3)H] glucose and Na-L-(+)-[U-14C] lactate. The infusion of endotoxin induced a transient hyperglycemic level, followed by a steady fall in plasma glucose to hypoglycemic levels. The rate of appearance (Ra) and the rate of disappearance (Rd) of glucose were both significantly elevated (P less than .05) for 150 min after endotoxin, after which neither differed from the preinfusion value. The metabolic clearance rate of glucose was significantly elevated at all times 30 min postendotoxin. By 30 min postendotoxin, Ra and Rd of lactate, plasma lactate concentration, and the percent of glucose turnover originating from lactate were significantly elevated and remained so for the duration of the experiment. We concluded that after endotoxin hypoglycemia developed because of an enhanced peripheral uptake of glucose and a failure of the liver to maintain an increased Ra of glucose. We also concluded that lactate became an important precursor for gluconeogenesis and an important metabolic substrate.

Animals↗
PubMed1977

Effect of burn injury on glucose turnover in guinea pigs.

Using our guinea pig model, we found the rate of appearance of glucose was elevated during the three phases following burn injury: the burn shock phase, the hypermetabolic phase and the septic phase. The rate of disappearance of glucose initially was not elevated, resulting in hyperglycemia during burn shock, but eventually, the rate of disappearance of glucose increased to the same extent as the rate of appearance of glucose. During the hypermetabolic and septic phases, the glucose turnover rate was elevated, but the plasma glucose concentration was normal. Glucose turnover was poorly correlated with total body oxygen consumption, suggesting that not all of the increased turnover of glucose was due to increased glucose oxidation.

Animals↗
PubMedDate not supplied

The effect of age on insulin response and glucose utilization during four hyperglycemic plateaus.

In order to evaluate the potential role of insulin insensitivity as a cause of the glucose (G) intolerance of aging, we performed 230 hyperglycemic clamps, 85 on young (Y, 24 to 39 years), 47 on middle age (M, 40 to 59 years), and 98 on old (O, 60 to 90 years) carefully screened subjects of the Baltimore Longitudinal Study of Aging. The 2-h plasma G levels on an oral glucose tolerance test (OGTT) were < 7.8 mmol/l in Y and M and < 10 mmol/l in old; the latter group was further dichotomized at 7.8 mmol/l into a "normal" group, ON, and an impaired group, OI. Four hyperglycemic plateaus were created: 3.0, 5.4, 7.9, and 12.8 mmol/l above basal. Three measures of glucose tolerance--1) G at 2 h after glucose ingestion, 2) glucose utilization, M, at each hyperglycemic plateau, and 3) glucose decay constant, K, obtained at the conclusion of each clamp--showed the best performance in the young group (Y > M = ON > OI). Despite these differences in glucose tolerance, plasma insulin responses (I) during the clamp were not significantly different except that ON < Y at the basal + 12.8 plateau (300 +/- 42 vs. 456 +/- 48 pmol/l, p < 0.01). Insulin-dependent glucose uptake, a measure of tissue sensitivity to insulin, was decreased in the old-impaired group at every plateau except the highest. We conclude that healthy, active older subjects showed moderate intolerance to oral and IV glucose and that the mechanism of this physiological aging process is most likely decreased insulin sensitivity.

Adult↗