Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of starvation on the hepatic glycogen synthase and phosphporylase systems were sequentially assessed in fed and 24-120-hr-fasted rats. Enzymic changes before and after glucose were correlated with simultaneous measurements of hepatic cyclic AMP and glycogen concentrations and glucose, insulin, and glucagon concentrations in the portal vein plasma. Fasting caused parallel changes in plasma glucose and hepatic glycogen concentrations with decreases by 24 hr and subsequent increases, which correlated with increases in hepatic synthase l and decreases in phosphorylase activites. Hepatic cyclic AMP levels increased as 24-48 hr, decreased below fed levels at 96 hr, and increased again at 120 hr. Fasting caused progressive impairment of glucose disposal, decreased basal and postglucose insulin concentrations, and decreased basal glucagon levels at 48-72 hr. Hepatic synthase l increments following glucose were exaggerated in 48-120-hr-fasted rats, although consistent phosphorylase decrements were seen only in fed rats. There was no clearcut relationship between synthase activation and phosphorylase inactivation following glucose in fed or fasted rats.
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PMID:Effect of starvation on hepatic glycogen metabolism and glucose homeostasis. 20 23

Glucagon is known to elevate the intracellular concentration of cyclic AMP in the hepatocyte. The increase in intracellular cyclic AMP is reflected by an increase in the plasma concentration of the nucleotide. Intravenous glucagon stimulation was performed on six obese non-diabetic human subjects before and after a three day fast. All patients responded to starvation by a lowering of plasma immunoreactive insulin and blood glucose. Whereas the plasma immunoreactive glucagon concentration increased over the three day period, the plasma and urinary cyclic AMP did not significantly change. Intravenous glucagon promoted qualitatively similar increases in the blood glucose and plasma concentrations of insulin and cyclic AMP before and after three days starvation.
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PMID:Urinary and plasma cyclic AMP levels during short term starvation in obese man: response to glucagon stimulation. 20 64

The effect of long-term starvation on glucagon-mediated hepatic glycogenolysis was investigated in the rat in vivo. Following glucagon (50 microgram/kg i.v.) fed rats showed rapid phosphorylase activation but no change in synthase-I activities. In contrast, rats fasted 72 hr (long-term fasting) showed rapid synthase inactivation but no significant phosphorylase activation. Rats fasted 24 hr (short-term fasting) demonstrated coordinated inactivation of synthase and activation of phosphorylase. Hepatic cyclic AMP responses were greater in fasted rats. Hepatic glycogen concentrations in rats fasted 72 hr were approximately 30% of fed levels. After glucagon, comparable decrements in hepatic glycogen and increments in plasma glucose concentrations were seen in fed and 72-hr groups. The diminished responsiveness of the hepatic phosphorylase system in rats fasted 72 hr was not attributable to altered cyclic AMP-dependent protein kinase or phosphorylase kinase activities. However, the diminished responsiveness could be ascribed to diminished total phosphorylase with nearly complete activation in the basal state. In fed and fasted rats, synthase decrements after glucagon correlated closely with basal levels of synthase-I. Thus, it is proposed that the enzymatic mechanism of glucagon-mediated hepatic glycogenolysis differs in fed and fasted rats. It is also proposed that partial hepatic glycogen reaccumulation during long-term fasting could be physiologically important for glucose homeostasis.
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PMID:Altered mechanism of glucagon-mediated hepatic glycogenolysis during long-term starvation in the rat. 21 68

Various hormonal and non-hormonal agents were tested for their ability to induce ornithine decarboxylase (EC 4.1.1.17) in primary cultures of fetal rat liver cells that retain many of the differentiated functions of hepatocytes. The only agents to induce ornithine decarboxylase in this cell type were fetal calf serum, prostaglandin E1 and cyclic AMP derivatives. Also, the amino acid arginine would induce ornithine decarboxylase in this cell type following arginine starvation for 24 h. These observations are in contrast to the wide range of hormones, e.g. insulin, hydrocortisone, glucagon and growth hormone, than can induce ornithine decarboxylase in vivo in the adult rat liver but which are all without effect on fetal rat liver cells.
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PMID:Factors regulating the induction of ornithine decarboxylase in fetal rat liver cells in culture. 21 27

Although the molecular basis of thyroid hormone action remains obscure, a growing body of evidence has suggested that triiodothyronine (T3) action is initiated at a set of specific nuclear receptor sites. The physiologic significance of these T3-binding sites is supported by four lines of evidence: 1) the high-affinity, limited-capacity binding of T3; 2) the relationship between binding affinity of thyroid hormone analogs and hormonal potency; 3) the correlation of concentration of nuclear receptor and physiologic response in various tissues; 4) the relationship between receptor occupancy and physiologic response. While the levels of hepatic nuclear receptor do not change in response to T3, recent evidence indicates receptor concentration is markedly reduced by partial hepatectomy, starvation, or administration of glucagon. This reduction results in a decrease in the response of malic enzyme to T3, but leaves the response of alpha-glycerol phosphate dehydrogenase unimpaired. Thus, specific control of thyroid responses by modulating receptor concentration may occur. Occupancy of hepatic receptors by T3 is associated with increases in both the rate of formation and steady-state concentration of poly(A)-containing mRNA. The values of these two parameters in the euthyroid rat liver were approximately 60--80% greater than values in hypothyroid animals. Analyses of the sequence and frequency complexity of poly(A)-containing mRNA from euthyroid and hypothyroid rats revealed no major changes in either the qualitative or quantitative distribution of mRNA sequences. Although it is recognized that the levels of certain specific species of mRNA (ie, alpha 2u-globulin) are altered as a result of thyroid hormone action, these data strongly indicate a concomitant generalized increase in the production of all major classes of mRNA.
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PMID:Interaction of thyroid hormones with target tissues: effects of hepatic mRNA population. 23 83

Hypergastrinemia and hyperglucagonemia follow portacaval shunt (PCS) or cirrhosis in man and experimental animals. The cause is unknown although portal diversion and hepatic dysfunction are suggested. In these studies transhepatic techniques were used to define the hepatic handling of basal and arginine-stimulated gastrin and glucagon levels in sham-operated and portacaval-shunted pigs and in a group of pair-fed sham-operated pigs. After PCS, basal gastrin levels were lower than those in sham-operated animals but were also lower in the pair-fed group, suggesting that the change resulted from partial starvation. Arginine-stimulation caused a rise in hepatic venous levels in PCS and in pair-fed pigs and in portal venous levels in sham-operated pigs. These data also suggested a response to diminished intake in PCS pigs. There was an immediate transitory rise in portal immunoreactive glucagon (Unger 30K) after PCS and a subsequent rise from the 4th postoperative day in all circulations. Arginine stimulation caused in sham-operated and PCS pigs a biphasic rise in the portal circulation and a later rise in the arterial circulation in PCS pigs. These data suggest that the effect of PCS upon gastrin levels is associated with the impaired appetite while the effect upon glucagon is the result of diversion past the liver.
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PMID:Transhepatic hormone levels in the portacaval shunted pig--the effects of arginine upon gastrin and glucagon release. 29 Feb 69

In the first part of the study oral glucose tolerance tests (GTT) or insulin tolerance tests (ITT) were performed in 22 lean and 22 obese nondiabetics before and after fasts of at least 6 days' duration. Deterioration of glucose tolerance was greater in lean than in obese individuals. Plasma levels of factors known to influence glucose tolerance (glucagon, growth hormone, free fatty acids, ketones) were significantly higher in fasting lean than in fasting obese subjects. Furthermore, delayed insulin rise (GTT) and decreased insulin sensitivity (ITT) were observed after starvation in lean subjects but not in the obese, which could explain the greater deterioration of glucose tolerance in the lean population. In the second part of the study glucose and fructose tolerance were compared during 4-hour infusions of these substrates (0.5 g/kg/h) in 8 normal subjects before and after two 4-day fasts. After starvation, glucose as well as fructose infusion resulted in plasma levels of the infused hexose significantly higher than in control, and the rise in plasma lactate and pyruvate was delayed. These results contradict the view widely held in the literature, that fructose metabolism remains unimpaired in the fasting state.
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PMID:[Carbohydrate intolerance during complete fasting]. 33 74

Mammalian pregnancy is characterized by progressive hyperinsulinaemia, raised plasma lipids and increased vulnerability to ketosis after food deprivation. The present investigations were performed to assess the role of two placental steroids, oestradiol and progesterone, in the development of these changes, since plasma titres of these hormones progressively increase during human gestation. In both human subjects and adult female rats it was demonstrated that these two steroids, separately or in combination, augment plasma insulin concentration in vivo, cause hypertrophy of pancreatic islets and promote exaggerated secretion of insulin, but not glucagon, by pancreatic islets in vitro. Hypertriglyceridaemia induced by oestrogen alone or combined with progesterone was associated with increased splanchnic production of triglyceride as well as altered tissue lipoprotein lipase (EC 3.1.1.34) and circulating apoproteins that influence activity of this enzyme. The combined regimen also increased hepatic glycogen storage and suppressed gluconeogenesis in vivo in the rat while accelerating the onset of ketosis during starvation in human subjects and in the animal model. Oestradiol and progesterone appear to effect metabolic changes in nonpregnant animals and human subjects that simulate maternal adaptations to advancing gestation, including altered endocrine pancreatic function, triglyceride metabolism and metabolic fuel storage and mobilization.
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PMID:The influence of hormonal changes of pregnancy on maternal metabolism. 37 20

1. Regulation of gluconeogenic substrate supply and modulation of the gluconeogenic pathway in the liver are both important in the control of gluconeogenesis by glucocorticoids. 2. Adrenal deficiency decreases the release of gluconeogenic and other amino acids from skeletal muscle during starvation. The effect is reversed by glucocorticoid replacement. The changes in amino acid release are accompanied by similar alterations in tissue amino acid levels and are not explained by alterations in net protein breakdown. Glucocorticoids do not alter protein catabolism and cause a small inhibition of protein synthesis. The biochemical alterations underlying the changes in amino acid metabolism induced by these steroids remain to be elucidated. Glucocorticoids may also regulate the supply of gluconeogenic substrates through permissive effects on the lipolytic action of catecholamines and other hormones in adipose tissue and on the glycogenolytic action of catecholamines on skeletal muscle. 3. Glucocorticoids are required for the increases in gluconeogenesis in starvation and diabetes. Part of their action is exerted directly on the liver and appears to involve modulation of P-enlopyruvate carboxykinase levels. Glucocorticoids increase the synthesis of this enzyme apparently through effects at the level of transcription. 4. Glucocorticoids exert permissive effects on the stimulation of gluconeogenesis in the liver by glucagon and epinephrine. The steroids are not required for cAMP generation or protein kinase activation by these hormones, but appear to act by maintaining the responsiveness of certain enzymes to the effects of the cAMP and alpha-adrenergic systems. It is proposed that this involves the maintenance of a normal intracellular ionic environment.
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PMID:Regulation of gluconeogenesis by glucocorticoids. 38 91

The responses of plasma gastro-entero-pancreatic (GEP) hormones and free fatty acids (FFA) to a standard mixed meal before and after starvation have been measured. Raised insulin, glucose and FFA levels were found following refeeding after starvation and levels of secretin and C-terminal glucagon-like-immunoreactivity (C-GLI), raised by starvation, were rapidly suppressed on refeeding. The responses of gastrin and N-terminal glucagon-like-immunoreactivity (N-GLI) to a standard mixed meal were not altered by starvation. Although this study does not directly support that secretin and glucagon are responsible for the hyperglycaemia or hyperinsulinaemia of starvation diabetes, a role for both hormones in the raised FFA levels is proposed, as well as a role for glucagon in the initial hyperglycaemic response to a meal after starvation.
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PMID:The gastro-entero-pancreatic hormone secretion after a mixed meal in normal subjects before and after a 72 hour period of starvation. 44 30


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