Effect of Growth Hormone Deficiency on Glucagon Secretion

Blackard, William G.; Andrews, Samuel S.; Lazarus, E. J.

doi:10.3181/00379727-143-37466

Cited by 10 publications

(5 citation statements)

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“…The present study demonstrates that plasma insulin response to arginine was diminished in isolated GH deficiency and almost normal in acromegaly (exaggerated in non-diabetic acromegalics and low in diabetic acromegalics). These findings have confirmed previous observations (Laron et al, 1967;Fineberg et al, 1970;Blackard et al, 1973;Sizonenko et al, 1975) and further demonstrated that plasma insulin response to arginine in acromegaly with severe diabetes is impaired. In the present experiments, we also found that fasting plasma glucagon level and plasma glucagon level following arginine infusion were significantly elevated in both patients with isolated GH deficiency and acromegaly.…”

Section: Discussionsupporting

confidence: 92%

“…In the present experiments, we also found that fasting plasma glucagon level and plasma glucagon level following arginine infusion were significantly elevated in both patients with isolated GH deficiency and acromegaly. Blackard et al (1973) and Sizonenko et al (1975) observed that in patients with growth hormone deficiency, plasma glucagon response to arginine tended to be slightly but not significantly higher than in normal subjects. However, in the experiments by Rlackard et al…”

Section: Discussionmentioning

confidence: 94%

“…These findings suggest that pituitary GH plays a physiological role in the capacity of the pancreas to secrete insulin. On the other hand, only a few studies (Goldfine et al, 1972;Blackard et al, 1973;Sizonenko et al, 1975) have been carried out about effect of endogenous GH on plasma glucagon release. In our previous study , we have reported non-suppressibility of plasma glucagon by orally administered glucose in acromegalic patients.…”

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confidence: 99%

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Growth Hormone Modulation of Arginine‐induced Glucagon Release: Studies of Isolated Growth Hormone Deficiency and Acromegaly

Seino

Taminato

Goto

et al. 1978

Clinical Endocrinology

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Plasma glucagon and insulin responses to L-arginine were compared in normal controls and patients with isolated growth hormone deficiency and acromegaly. Patients with isolated growth hormone deficiency were characterized by high plasma glucagon response and low plasma insulin response, whereas acromegalic patients showed exaggerated plasma glucagon response and almost normal insulin response. These results suggest that growth hormone is probably required for optimum function of the islets, and since hyperglucagonaemia was observed in both growth hormone deficiency and acromegaly, metabolic disturbances stemming from the respective primary diseases may affect glucagon secretion.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 94%

mentioning

confidence: 99%

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Growth Hormone Modulation of Arginine‐induced Glucagon Release: Studies of Isolated Growth Hormone Deficiency and Acromegaly

Seino

Taminato

Goto

et al. 1978

Clinical Endocrinology

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“…to be decreased in subjects with growth hormone deficiency (8,13,18,39,41). Effects of growth hormone on pancreatic oc cell function have only recently been reported (5,20). The aim of the present experiments was to test pancreatic glucagon as well as insulin responsiveness in children and adolescents with deficiency of growth hormone secretion, and in others with idiopathic short stature or anorexia nervosa.…”

mentioning

confidence: 92%

Plasma Growth Hormone, Insulin, and Glucagon Responses to Arginine Infusion in Children and Adolescents with Idiopathic Short Stature, Isolated Growth Hormone Deficiency, Panhypopituitarism, and Anorexia Nervosa

et al. 1975

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ExtractThe effects of intravenous infusion of arginine (20 g/m2) after an overnight fast on plasma immunoreactive growth hormone (GH), insulin (IRI), and glucagon (IRG), and blood glucose were examined in five groups of children and adolescents: 10 normal individuals, 18 with idiopathic short stature, 6 with isolated growth hormone deficiency, 8 with panhypopituitarism, and 6 with anorexia nervosa.The mean fasting plasma GH concentration was significantly elevated in the group with anorexia nervosa (P < 0.05), and similar to the value for the normal group in all other groups. After arginine infusion, four-to sixfold increases of plasma G H were observed in the normal children, and similar increases were seen in those with idiopathic short stature as well as in those with anorexia nervosa; whereas, in the children with isolated growth hormone deficiency or panhypopituitarism, there was no significant increase in plasma GH. Fasting blood glucose concentrations were significantly lower than normal in subjects with isolated growth hormone deficiency ( P < 0.05), panhypopituitarism ( P < 0.001), and anorexia nervosa (P < 0.001), whereas fasting plasma IRI and IRG concentrations were similar to the values in the normal group. Plasma IRI increased eightfold at the end of the 30-min arginine infusion in the normal subjects; the increase was slightly but not significantly less in those with idiopathic short stature, and significantly less in those with isolated growth hormone deficiency ( P < 0.05), panhypopituitarism ( P < 0.001), and anorexia nervosa ( P < 0.05). Arginine infusion resulted in two-to threefold increases of plasma IRG in the normal group, and similar increases were observed in all of the other groups tested. These results suggest that whereas pancreatic P cell responsiveness may be deficient in children and adolescents with isolated growth hormone deficiency, panhypopituitarism, or anorexia nervosa, pancreatic a cell responsiveness, to arginine a t least, appears to be intact under these conditions. SpeculationAlthough plasma glucagon responses to arginine infusion were not less in subjects with hypopituitarism or anorexia nervosa than in normal subjects, relative hypoglucagonemia may have existed, since both basal and postarginine infusion plasma glucagon levels were not higher than normal in the presence of significantly lower blood glucose values. Thus, the present study does not exclude a deficient pancreatic a cell response to hypoglycemia. Alternatively, nonavailability of substrates for gluconeogenesis may have a more important influence than hormonal factors in the genesis of the hypoglycenia observed in these states.73

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“…This combination of growth and functional deficiency suggests the malfunction of a negative feedback for a hypothetical insulotrophic factor: a situation comparable to the TSH-induced enlargement of the thyroid following pharma cologic block of thyroid hormone biosynthesis. A prime suspect in the produc tion of this factor is the anterior pituitary, since hypopituitarism is associated with decreased B cell activity and hypoinsulinism (1,13,22,30), while pituitary hyperfunction, pituitary extracts and especially growth hormone, increase the size and granule content of the B cells in hypophysectomized animals (22,30), and stimulate the secretion of insulin (6), even though they may induce diabetes (2,25). The relationship between anterior pituitary and A cells is less clear.…”

Section: Introductionmentioning

confidence: 99%

Secretion of Glucagon and Insulin in Hypophysectomized Rats: Effect of Tolbutamide

Dunbar¹,

Walsh²,

Foà³

1979

Horm Res

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Normal and hypophysectomized (hypox) rats, fed ad libitum, received intraperitoneal injections of tolbutamide (75 mg/kg/day) or of saline for 6 weeks. 24 h after the last injection, blood samples were taken for glucose, insulin and glucagon determinations. In normal rats, tolbutamide treatment did not alter serum glucose, insulin and glucagon, although it suppressed the secretion of insulin and glucagon by the pancreatic islets. In hypox rats, tolbutamide decreased serum glucose and insulin, elevated serum glucagon and stimulated the secretion of glucagon, but not that of insulin by the pancreatic islets. In addition, tolbutamide treatment increased the glucagon response to arginine in normal, but not in hypox rats. The serum glucose response to arginine was decreased by tolbutamide treatment and by hypophysectomy and, thus, appeared independent of the glucagon rise or preexisting glucagon level. We conclude that tolbutamide treatment decreased the secretion of glucagon and insulin in normal rats and stimulated that of glucagon in hypox rats, perhaps because of the low levels of insulin in the serum and in the pancreas of the latter. Our results are compatible with the hypothesis that the pancreatic action of tolbutamide is influenced by the pituitary.

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Effect of Growth Hormone Deficiency on Glucagon Secretion

Cited by 10 publications

References 1 publication

Growth Hormone Modulation of Arginine‐induced Glucagon Release: Studies of Isolated Growth Hormone Deficiency and Acromegaly

Growth Hormone Modulation of Arginine‐induced Glucagon Release: Studies of Isolated Growth Hormone Deficiency and Acromegaly

Plasma Growth Hormone, Insulin, and Glucagon Responses to Arginine Infusion in Children and Adolescents with Idiopathic Short Stature, Isolated Growth Hormone Deficiency, Panhypopituitarism, and Anorexia Nervosa

Secretion of Glucagon and Insulin in Hypophysectomized Rats: Effect of Tolbutamide

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