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Biomedical subjects

J W Ensinck

Publications and source records attributed to J W Ensinck.

At least 55 records · Page 3Linked to original sources
PubMed1979

Evaluation of the control of glucagon secretion by the parasympathetic nervous system in man.

To evaluate the influence of the parasympathetic nervous system on human glucagon secretion, we have measured the plasma immunoreactive glucagon (IRG) levels after the administration of edrophonium, bethanechol chloride, and 2-deoxyglucose, and have compared the IRG responses to hypoglycemia in normal, atropinized, and vagotomized man. Edrophonium administered i.v. and bethanechol chloride administered s.c. did not affect IRG levels. Two-deoxy-glucose resulted in symptomatic neuroglucopenia with resultant vagal discharge, as evidenced by increased gastric acid secretion; but no changes in IRG concentrations were observed. The IRG response to insulin-induced hypoglycemia in normal subjects was not influenced by the administration of atropine. In seven subjects with a truncal vagotomy and no increased gastric acid secretion during insulin-induced hypoglycemia, the IRG increases were indistinguishable from those of control subjects in terms of timing, peak level obtained, or total glucagon response. We conclude that the cholinergic system is unlikely to play an important role in modulating glucagon secretion in man.

Adult↗
PubMed1979

Reduction of plasma triglyceride concentration by acute stress in man.

Three different forms of stress all resulted in acute reduction of plasma triglyceride concentrations. Pyrogen reactions in two hypertriglyceridemic men resulted in the lowering of very-low-density lipoprotein (VLDL) triglyceride levels by 93% and 73% due to decreased secretion of this lipoprotein into plasma. More modest reductions in plasma triglycerides were observed after 2-deoxyglucose-induced intracellular glucopenia and insulin-induced hypoglycemia. With hypoglycemia, the lowering of plasma triglyceride concentration correlated significantly with the stimulation of urinary epinephrine output (r = 0.86) but with neither the urinary norepinephrine response nor with the increase in plasma immunoreactive glucagon levels. To further test whether these changes in plasma triglyceride levels were mediated via the sympathetic nervous system, hypoglycemia was evoked by insulin in subjects with traumatic spinal cord transactions. Two such subjects, who demonstrated sympathetic stimulation in response to hypoglycemia, had evidence of reduced VLDL secretion into plasma, while in two who had no evidence of an adrenergic response. VLDL secretion was not inhibited. Thus, acute lowering of plasma triglyceride concentrations by certain forms of stress appears to be mediated via the sympathetic nervous system.

Acute Disease↗
PubMed1978

Dominant inheritance of large molecular weight immunoreactive glucagon.

Plasma from some individuals contains substances which are reactive with glucagon antiserum, are larger than 3,500-dalton glucagon, and have been proposed as possible precursors of glucagon. We have evaluated three generations of a kindred in which 9 of 15 members evaluated had elevated plasma levels of large molecular weight immunoreactive glucagon (L-IRG) with an average concentration of 822 pg/ml. The distribution of individuals with elevated L-IRG levels in this pedigree is consistent with autosomal dominant inheritance. Gel filtration of plasma revealed that all affected family members had excessive amounts of two L-IRG peaks, one with a molecular weight of approximately 9,000 daltons and another in the 10,000 to 20,000-dalton range. Oral glucose tolerance tests were nondiabetic and elicited a fall in L-IRG levels, whereas L-IRG concentrations rose dramatically during the infusion of arginine. These L-IRG species may be precursors of 3,500-DALTON GLUCAGON AND MAY BE ELEVATED in this kindred because of an inherited defect in either their synthesis or degradation.

Adolescent↗
PubMed1977

Insulin, glucagon, and glucose exhibit synchronous, sustained oscillations in fasting monkeys.

In overnight fasted rhesus monkeys, synchronous, regular oscillations occurred in the plasma concentrations of glucose, insulin, and glucagon. The oscillations displayed a period averaging 9 minutes. The amplitudes for insulin and glucagon were ten and five times greater than for glucose. Insulin cycled in and glucagon out of phase with glucose. In baboons, oscillations of glucose and insulin were smaller than in rhesus monkeys, while in man, regular oscillations were not observed.

Animals↗
PubMed1977

Phentolamine prevents the somatostatin-mediated inhibition of pancreatic glucagon secretion.

This study was undertaken to assess the role of alpha-adrenergic receptors in the somatostatin-mediated inhibition of pancreatic glucagon secretion. In dogs, somatostatin inhibited the pancreatico-duodenal vein output of glucagon. During an infusion of the alpha-adrenergic blocking agent phentolamine, somatostatin did not significantly inhibit the output of glucagon. Thus, alpha-adrenergic mechanisms appear to influence the ability of somatostatin to decrease pancreatic glucagon secretion.

Animals↗
PubMed1977

Insulin and glucagon relationship during aging in man.

To determine if the glucoregulatory hormones, insulin and glucagon, are altered with aging inman, 44 healthy volunteers, 22-81 yr of age, were evaluted by measurement of basal levels of glucose, insulin, and glucagon in relationship to their fat mass. In addition, the secretory capacities of the alpha and beta cells were assessed by measurement of the amounts of glucagon and insulin released after intravenous administration of glucose and arginine, respectively. Although no significant differences in weight could be distinguished longitudinally, the percentage adiposity was found to increase with age. Basal concentrations of glucose, glucagon, and insulin were not appreciably altered as a function of advancing years. After intravenous glucose, the glucose disappearance rate (Kg) was significantly slower in the elderly in comparison with the young, yet no differences in glucose-induced release were found. Similarly, insulin responses after arginine infusion between young and old were indistinguishable. The release of glucagon in response to arginine infusion was not perceptibly altered during aging. Thus, despite a decline in Kg with advanging age in this healthy population, gross changes in insulin and glucagon release were not apparent. We infer from bese data that decreased carbohydrate tolerance accompanying aging in some populations may be due to factors other than abnormalities in secretion of insulin and glucagon.

Adipose Tissue↗
PubMed1977

Role of glucagon in mediating metabolic effects of epinephrine.

In order to separate direct effects of epinephrine on fuel metabolism from those mediated by glucagon, epinephrine (0.1 microng/kg-min) was infused for 120 min in 18- and 65-h fasted, nonanesthetized baboons with and without a concomitant somatostatin infusion. At both stages of fasting, epinephrine stimulated glucagon, secretion, and this was blocked by somatostatin. At 18 h, with epinephrine alone, glucose rose early and remained elevated throughout the infusion. In the glycogen-depleted 65-h fasted animals, there was attenuation of the early glucose rise, with glucose reaching a maximum level at 100-120 min. With somatostatin blockade of glucagon release in the 18-h fasted animals, a pattern of attenuated early glucose rise similar to that of the 65-h fasted animals occurred. Somatostatin also inhibited this early glycogenolytic response when the epinephrine dose was increased fivefold. The behavior of FFA, glycerol, and beta-hydroxybutyrate was unchanged by the addition of somatostatin to epinephrine at either stage of fasting. Thus, glucagon mediates the early glycogenolytic response to epinephrine, but not the delayed hyperglycemia and probably not the lipolysis.

Animals↗
PubMed1977

Glucagon and catecholamine secretion during hypoglycemia in normal and diabetic man.

To examine the role of catecholamines in glucopenia-induced glucagon secretion, urinary epinephrine and norepinephrine and plasma immunoreactive glucagon (IRG) were measured during insulin-induced hypoglycemia in normal and insulin-dependent diabetic-man. Despite equivalent levels of hypoglycemia the mean plasma IRG increment in diabetes was only 15% of normals. The increases in epinephrine and norepinephrine were comparable in diabetics and normals; thus, the blunted response in plasma IRG to the stimulus of low blood sugar in diabetics cannot be explained by a generalized defect in catecholamine secretion. It is suggested that an alpha-cell glucoreceptor defect may account for the abnormal response to glucopenia in diabetics. To evaluate the possibility that impaired sensitivity to circulating catecholamines could explain the alpha cell dysfunction in diabetics, exogenous epinephrine was infused in normals and insulin-dependent diabetics. Elevated plasma IRG during epinephrine infusion was observed in only 50% of normals. The diabetics were hyperresponsive; mean increment in plasma IRG 3 times that of normals. The data demonstrate enhanced rather than impaired sensitivity to catecholamines in diabetes mellitus.

Adolescent↗
PubMed1976

Glucagon responses to hypoglycemia in adrenalectomized man.

In order to examine the possibility that epinephrine is involved in either the mediation or modulation of the enhanced glucagon release during glucopenia, glucagon responses to insulin-induced hypoglycemia were evaluated in four men with bilateral adrenalectomy in comparison with ten normal men. In the adrenalectomized patients, the mean nadir of plasma glucose and the rate of ascent to baseline levels were indistinguishable from those observed in normal subjects. Similarly, glucagon responses in the adrenalectomized group were not different from those encountered in the normal volunteers. We conclude that epinephrine does not contribute significantly to the augmented glucagon release during abrupt glucopenia in normal man and is not necessary for normal recovery from hypoglycemia.

Adolescent↗
PubMed1976

Mechanism of plasma cyclic AMP response to hypoglycemia in man.

The effect of insulin-induced hypoglycemia on plasma cyclic AMP levels was studied in normal volunteers, adrenalectomized, and sympathectomized subjects. Significant increases in plasma glucagon were observed in all groups. Normal subjects all had two- to threefold rises in plasma cAMP while no response was seen in any adrenalectomized or sympathectomized subject. These findings suggest that the mechanism for enhanced plasma cAMP release during insulin-induced hypoglycemia is catecholamine dependent. Glucagon does not contribute significantly to this response.

Adrenalectomy↗
PubMed1976

Dominant inheritance of large molecular weight species of glucagon.

Excessive plasma levels of high molecular weight (MW) components of immunoreactive glucagon (IRG) have been found in three generations of a family in a pattern consistent with an autosomal dominant trait. Preliminary studies using gel filtration suggest the presence of two MW species of IRG greater than 3500 daltons in plasma of affected members who have normal oral glucose tolerance tests. The "hyperglucagonemia" in this pedigree is consonant with either a structural defect in biosynthetic precursors or an abnormality in enzyme-mediated cleavage of proglucagon.

Adolescent↗