Insulin and glucagon secretion was ..
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but not glucagon, stimulates OGT synthesis and ..
T1 - Stimulation of HTC hepatoma cell growth in vitro by hepatic stimulator substance (HSS). Interactions with serum, insulin, glucagon, epidermal growth factor and platelet derived growth factor
Both insulin and glucagon stimulate ..
AB - Hepatic stimulator substance (HSS), a partially purified extract of weanling or regenerating adult rat liver, is an organ-specific stimulator of liver growth in vivo and in vitro. The HTC hepatoma cell line is particularly responsive to HSS. The present experiments show that HSS will stimulate HTC cells in the complete absence of serum, although graded doses of fetal cal serum (FCS), from 0.1 to 5.0%, will increase the degree of stimulation in a dose-dependent manner. In contrast, when HSS is absent, increasing doses of FCS above 0.5% inhibit DNA synthesis. Much of this inhibition is removed by prior dialysis of the FCS and maximum enhancement of the HSS-induced stimulation occurs with only 0.1-0.5% of the dialysed FCS. Sera from older animals have less or even negative effect. Evidence is presented to show that the enhanced stimulation by HSS in the presence of serum is not due to insulin, glucagon, epidermal growth factor (EGF), or platelet derived growth factor (PDGF) and that HSS does not act via a shared receptor for one of these hormones. These experiments provide further evidence that HSS is a unique stimulator of liver growth and lend support to a model of organ-specific growth control.
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Chronic kidney disease (CKD) | McMaster …
56. Yeung CM, Mojsov S, Mok PY, Chow BKC. Isolation and structure-function studies of a glucagon-like peptide 1 receptor from goldfish Carassius auratus: Identification of three charged residues in extracellular domains critical for receptor function. 2002;143:4646-54
28/09/2006 · Original Article
Leptin is a peripheral satiety hormone that also plays important roles in energy homeostasis in vertebrates ranging from fish to mammals. In teleost fish, however, the regulatory mechanism for leptin gene expression still remains unclear. In this study, we found that glucagon, a key hormone in glucose homeostasis, was effective at elevating the -AI and -AII transcript levels in goldfish liver via both intraperitoneal injection and cells incubation approaches. The responses of -AI and -AII mRNA to glucagon treatment were highly comparable. In contrast, blockade of local glucagon action could reduce the basal and induced -AI and -AII mRNA expression. The stimulation of leptin levels by glucagon was caused by the activation of adenylate cyclase (AC)/cyclic-AMP (cAMP)/ protein kinase A (PKA), and probably cAMP response element-binding protein (CREB) cascades. Our study described the effect and signal transduction mechanism of glucagon on leptin gene expression in goldfish liver, and may also provide new insight into leptin as a mediator in the regulatory network of energy metabolism in the fish model.