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)

Recently, it was shown that lipoprotein lipase (LPL) was produced in neonatal but not in adult rat liver. In an attempt to further define the mechanism involved in liver LPL expression, we identified a neonatal mouse hepatoma cell line, BWTG3, capable of producing LPL. The regulation of LPL expression by various extracellular stimuli was investigated in this cell line. Progesterone caused a rise in LPL production by BWTG3 cells. Other hormones tested, such as insulin, glucagon, adrenalin, testosterone, and thyroid hormone, had no effect on LPL production. The effects of progesterone on LPL production showed slow kinetics reaching a maximum 24 h after addition. Cotransfection of a progesterone receptor expression vector with a 5'-LPL-CAT reporter construct resulted in an induction of CAT activity, suggesting that the increase in LPL accumulation after progesterone was linked to transcriptional induction of the LPL gene. Stimuli causing an elevation of protein kinase A activity in the cells also increased LPL production. Three agents capable of elevating intracellular cAMP levels, i.e., forskolin, dBcAMP, and choleratoxin, caused an elevation of LPL production. The increase in LPL activity caused by forskolin and choleratoxin was paralleled by an elevation of LPL mRNA levels, while dBcAMP only induced a small elevation of LPL mRNA levels. The increase in LPL production was shown to be linked to the stimulation of the PKA signal transduction pathway and was apparently transmitted via the transcription factor CREB. No effect of the stimulation of protein kinase C or calcium/calmodulin-dependent kinase on LPL production was detected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lipoprotein lipase expression in undifferentiated hepatoma cells is regulated by progesterone and protein kinase A. 132 33

Progesterone receptors (PgR) have been immunocytochemically localized in the nuclei of several (40% to 75%) endocrine cells of the human pancreas and in a more variable number of neoplastic cells of 7 of 18 endocrine pancreatic tumors. Conversely the exocrine epithelial cells of the pancreas did not exhibit any PgR immunoreactivity in normal as well as in different pathologic conditions, including pancreatic adenocarcinomas. Estrogen receptors were not detected in any of the pancreatic samples investigated. Double immunocytochemical experiments have documented that PgR immunoreactivity in normal Langerhans islets is a consistent feature of most (75%) glucagon-producing A cells, of approximately 5% to 20% of insulin-producing B cells, and of a variable percentage of pancreatic polypeptide (PP)-producing cells, ranging from 5% to 70%. These figures were not affected by the sex, age, or underlying disease of the patients. The reported findings corroborate previous clinical and experimental evidence indicating that sex steroid hormones may have some regulatory effects on the functional activity of the endocrine pancreas.
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PMID:Immunocytochemical localization of progesterone receptors in endocrine cells of the human pancreas. 224 Jan 68

Insulin is the primary short-term hormonal regulator of metabolism in the resting ruminant. The concentration of plasma insulin is positively correlated with energy intake. Diets producing hyperinsulinaemia, direct the balance towards body gain (anabolic). However, in lactating animals, the postprandial rise in insulin is reduced, thereby favouring movement of nutrients to the mammary gland and promoting gluconeogenesis. Similar mechanisms balance the demands of foetal and maternal growth. Glucagon, on the other hand, stimulates both glycogenolysis and gluconeogenesis in the liver from glucogenic amino acids, thereby indirectly diminishing protein synthesis in muscle. Homeorhetic hormones from both the pituitary and reproductive glands, play a major role in the long-term control of nutrient partitioning. Oestrogens appear to affect feed intake, promote RNA and protein synthesis and inhibit gluconeogenesis in the liver, thereby promoting the metabolic adaptations necessary for pregnancy. Progesterone, on the other hand, appears to block the action of the oestrogens at cellular level, and may actually increase feed intake. The pituitary hormones, prolactin and somatotropin, bring about significant improvements in production, especially in milk yield. The action of the somatomedins appears to be responsible for the paradoxical spectrum of effects attributed to somatotropin.
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PMID:A review of energy metabolism in producing ruminants. 2. Control of nutrient partitioning. 228 91

Insulin stimulates lipogenesis by 100% for 5 h by a covalent modulation of acetyl-CoA carboxylase, and by 200% for 24 h by increasing malic enzyme and fatty acid synthase enzymic activities in brown-adipocyte primary cultures. At short times, noradrenaline and isoprenaline decrease lipogenesis. However, phenylephrine and glucagon have no effect. At long times, dexamethasone inhibits lipogenesis. This effect is precluded in the presence of insulin. Progesterone and tri-iodothyronine, alone or in the presence of insulin, produce a stimulation of the rates of lipogenesis.
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PMID:Hormonal regulation of rat foetal lipogenesis in brown-adipocyte primary cultures. 304 67

Rates of lipogenesis in foetal isolated brown adipocytes from 22-day-pregnant rats were significantly increased by lactate plus pyruvate as major substrates in the incubation medium, in comparison with the endogenous rates. Insulin stimulated foetal brown-adipocyte lipogenesis, and adrenaline or noradrenaline and isoprenaline decreased lipogenesis. Glucagon had no effect on the lipogenic rate in brown adipocytes. Progesterone administration to the mother significantly increased the rates of lipogenesis in brown adipose tissue and in isolated brown adipocytes from 22-day foetuses. Prolongation of gestation by progesterone to day 23 decreased the rates of brown-adipose-tissue lipogenesis in vivo and in isolated cells in the post-mature foetuses.
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PMID:Regulation of rat foetal lipogenesis in brown adipose tissue in vivo and in isolated brown adipocytes during the last day of, and after prolonged, gestation. 330 66

Seventy-eight Holstein cows alternately were assigned at calving to receive beta-carotene supplementation or act as controls to determine effects of beta-carotene on reproduction and carotene, luteinizing hormone, progesterone, insulin, glucose, and glucagon concentrations in blood plasma. Cows were fed a corn silage-based complete ration. Biweekly jugular blood samples were collected beginning the week after parturition through 90 days. At day 30, supplemented cows received 600 mg synthetic beta-carotene daily for 60 days. Plasma carotene reached a peak of 2.45 micrograms/ml compared to 1.50 micrograms/ml in controls. Supplementation significantly increased plasma carotene but had no effect on luteinizing hormone, progesterone, insulin, glucose, glucagon, or reproductive measures. Days to first heat, days to first breeding, days open, and services per conception averaged 74, 74, 95, and 1.7 for supplemented cows and 64, 76, 102, and 1.9 for control cows. Progesterone increased as lactation progressed. Somatic cells were not different between supplemented and control cows. Supplementation of beta-carotene did not improve reproductive efficiency or alter luteinizing hormone, progesterone, insulin, glucose, or glucagon in blood plasma or affect somatic cells in milk.
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PMID:Reproductive and metabolic characteristics of dairy cattle supplemented with beta-carotene. 637 92

It is well known that several amino acids, such as arginine, are potent stimuli for insulin and glucagon secretion from the pancreas. Recently, vagal arginine sensors, which modulate arginine-induced pancreatic hormone secretion, have been reported to exist in the liver. The present investigation was designed to evaluate the role played by gluconeogenesis in this hepatic influence. To this end, we studied the effects of an intraperitoneal injection of 3-mercaptopicolinic acid (3-MPA), a gluconeogenic inhibitor, on the pancreatic hormonal response induced by intraperitoneal administration of arginine (1 g/kg body mass) to hepatic vagotomized and sham vagotomized rats. Fifteen min following the injection of arginine, the increases in glucose and insulin concentrations were significantly lower in rats with an inhibited gluconeogenesis than in rats with an intact capacity for gluconeogenesis. There were no effects of the hepatic vagotomy on the arginine-induced hormonal responses either with or without the 3-MPA injection. The results suggest that gluconeogenesis is implicated in the hepatic modulation of arginine-induced pancreatic hormone secretion.
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PMID:Effect of inhibition of gluconeogenesis on arginine-induced insulin secretion. 777 20

Treatment of cyclic and pregnant rats with progesterone stimulates cell proliferation within the islets of Langerhans. It was investigated whether this effect of progesterone depends on sex and/or the presence of the gonads or the presence of oestradiol. For this purpose, Silastic tubes containing progesterone were inserted s.c. in intact and gonadectomized male and female rats, and in gonadectomized female rats treated with oestradiol. After 6 days of progesterone treatment, rats were infused for 24 h with 5-bromo-2'-deoxyuridine (BrdU) and dividing cells were identified in pancreatic sections by immunostaining for BrdU. Progesterone treatment increased islet-cell proliferation in intact male and female rats (P < 0.05), but not in gonadectomized male and female rats or in gonadectomized female rats supplemented with oestradiol. Furthermore, in intact male and female rats, progesterone treatment also stimulated cell proliferation in extra-islet pancreatic tissue (P < 0.05). Identification of the proliferating cells, by double-immunocytochemistry, revealed that progesterone treatment stimulated proliferation of both alpha and beta cells within the pancreatic islets. In extra-islet pancreatic tissue, progesterone treatment stimulated proliferation in both duct (cytokeratin 20-immunoreactive) and non-duct cells. Progesterone treatment did not increase the number of single glucagon or insulin-containing cells outside the pancreatic islets, nor that of cytokeratin 20/insulin double-positive cells, suggesting that progesterone treatment did not stimulate differentiation of duct cells into endocrine cells. Progesterone treatment did not affect insulin responses to an i.v. glucose load (0.5 g/kg body weight). It is concluded that progesterone stimulates pancreatic cell proliferation indirectly; gonadal factor(s), not identical to oestradiol, is (are) probably involved.
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PMID:Progesterone stimulates pancreatic cell proliferation in vivo. 1021 22

Factors that affect progesterone clearance from plasma and by hepatocytes in culture were examined in a series of experiments. In Exp. 1, the objective was to determine whether an increase in hepatic portal blood acetate or propionate could alter progesterone metabolism by the liver. For ewe lambs gavaged orally with sodium propionate compared with those gavaged orally with sodium acetate, serum progesterone concentrations began to diverge as early as 0.5 h after administration and were greater (P < 0.05) at 3 and 4 h after administration. The objective of Exp. 2 was to determine the effect of a single oral gavage of either sodium acetate or sodium propionate on peripheral insulin and glucagon concentrations. Ewes gavaged orally with sodium propionate had greater (P < 0.05) insulin concentrations at 0.5 and 1 h after gavage than ewes gavaged with sodium acetate. Furthermore, glucagon concentrations were greater (P < 0.05) at 0.5, 1, and 2 h for ewe lambs gavaged orally with sodium propionate compared with those receiving sodium acetate. The third experiment investigated the rate of in vitro progesterone clearance by cultured hepatocytes in response to treatment with different concentrations of insulin and glucagon. Progesterone clearance was reduced (P < 0.05) with the addition of 0.1 nM insulin compared with the control. Furthermore, there was a greater reduction (P < 0.05) in progesterone clearance in response to 1.0 and 10 nM insulin compared with the control and 0.1 nM insulin. No change was observed in progesterone clearance in hepatocytes treated with either physiological (0.01 and 0.1 nM) or supraphysiological (1.0 nM) glucagon. Supraphysiological concentrations of glucagon (1.0 nM) negated the effects of either 0.1 or 1.0 nM insulin on progesterone clearance by hepatocytes. However, with physiological concentrations of glucagon (0.1 nM) and 1.0 nM insulin, glucagon was not able to negate the reduction in progesterone clearance caused by insulin. These data are consistent with a paradigm in which elevated hepatic portal vein propionate increases plasma insulin in ruminants, which decreases progesterone clearance, thereby increasing serum progesterone concentrations.
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PMID:Diet-induced alterations in progesterone clearance appear to be mediated by insulin signaling in hepatocytes. 1661 12