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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The concentrations of total protein (TP), albumin and globulin in the blood serum were investigated in seven trials with 203 piglets weaned at the age of three to four weeks. The lowest values were recorded in the newborn piglets just before colostrum intake. Two days later the TP level was three times higher and that of globulin almost five times higher. Later the levels began to sink (more intensively in globulin) and the decrease lasted until the end of the second month of age. Albuminaemia increased from birth until the end of study (the beginning of the third month) without any greater influence of colostrum intake and at a rate reduced by weaning. The albumin-globulin quotient, the lowest on the second day of life, increased step by step. The better-growing piglets mostly had higher albuminaemia and their hypoglobulinaemia reached a normal level sooner after weaning as compared with the tail-enders. This suggests that nutrition, body growth and albumin and globulin synthesis are interdependent in piglets. An increase in serum corticosteroids induced by two days of starvation or two administrations of adrenocorticotropic hormone, caused an insignificant increase in the concentration of albumin. Two hours after ACTH administration, the high level of corticosteroids was not observed to be accompanied by a change in serum proteins.
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PMID:[Changes in blood protein levels in piglets during development and during stress]. 301 69

The hypothesis that the stimulatory action of free fatty acids (FFA) in the hypothalamic-pituitary-adrenocortical (HPA) axis occurs in part at the adrenal cortex was evaluated. Pathophysiological concentrations of oleic and linoleic acids, but not stearic or caprylic acid, stimulated steroidogenesis from cultured rat adrenocortical cells (concentrations eliciting 50% of maximal responses, approximately 60 and 120 microM, respectively), with a latency of 90 min. Maximal stimulation of steroidogenesis by both acids was < 50% of that produced by adrenocorticotropic hormone (ACTH) and was blocked by cycloheximide. The maximal steroidogenic response to ACTH was inhibited approximately 50% by oleic acid. The actions of oleic and linoleic acids were not associated with an increase in adenosine 3',5'-cyclic monophosphate (cAMP) secretion but appeared to require intracellular oxidation. None of the lipids influenced cell viability or corticosterone radioimmunoassay. The latency of the steroidogenic response, the putative requirement for intracellular oxidation, and the apparent lack of involvement of cAMP suggest a mechanism of action of FFA distinct from that of ACTH, yet still requiring protein synthesis. It is concluded that the modulation of steroidogenesis by these abundant naturally occurring lipids may be an important component of the control mechanisms within the HPA pathway in disorders of lipid homeostasis (e.g., obesity, starvation, or diabetes).
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PMID:Stimulation of steroidogenesis in cultured rat adrenocortical cells by unsaturated fatty acids. 761 25

Virtually every metabolic disorder characterized by elevated plasma free fatty acid (FFA) levels is also associated with hypercorticoidism. For example, the glucocorticoid response to insulin-hypoglycemia is shown in this report to be greatly potentiated in Type I diabetic rats. Since glucocorticoids (corticosterone, in rats) potentiate lipolysis and promote gluconeogenesis, they exacerbate diabetes. We found that elevation of circulating FFA levels in normal rats (via Intralipid/heparin infusion) increased plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone, and resulted in hyperglycemia. In vitro, however, cultured pituitary cells were relatively unaffected by FFA except at very high concentrations. Neither basal ACTH secretion nor the ACTH response to corticotropin-releasing hormone (CRH) was affected by pathophysiological molar ratios of FFA:BSA. Thus, the ACTH secretory response to FFA in vivo likely is mediated via neuroendocrine activation. Cultured adrenocortical cells, however, were stimulated by oleic acid and, to a lesser extent, by linoleic acid; saturated fatty acids were without effect. The latencies of oleic acid-induced steroidogenesis in vitro and Intralipid-induced corticosterone secretion in vivo were both about 60 min. We conclude that pathophysiological levels of circulating FFA (typical of diabetes, obesity, starvation, and consumption of high-fat diets) initiate a positive feedback loop between the adipocyte and the HPA axis, which ultimately exacerbates the symptoms of these disorders.
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PMID:Regulation of pituitary-adrenocortical activity by free fatty acids in vivo and in vitro. 778 56

The adrenocorticotropic hormone (ACTH) inhibits the growth of Y1 mouse adrenocortical tumor cells as well as normal adrenocortical cells in culture but stimulates adrenocortical cell growth in vivo. In this study, we investigated this paradoxical effect of ACTH on cell proliferation in Y1 adrenal cells and have unmasked a growth-promoting effect of the hormone. Y1 cells were arrested in the G1 phase of the cell cycle by serum starvation and monitored for progression through S phase by measuring [3H]thymidine incorporation into DNA and by measuring the number of nuclei labeled with bromodeoxyuridine. Y1 cells were stimulated to progress through S phase and to divide after a brief pulse of ACTH (up to 2 h). This effect of ACTH appeared to be cAMP independent, since ACTH also induced cell cycle progression in Kin-8, a Y1 mutant with defective cAMP-dependent protein kinase activity. The growth-promoting effect of ACTH in Y1 was preceded by the rapid activation of p44 and p42 mitogen-activated protein kinases and by the accumulation of c-FOS protein. In contrast, continuous treatment with ACTH (14 h) inhibited cell cycle progression in Y1 cells by a cAMP-dependent pathway. The inhibitory effect of ACTH mapped to the midpoint of G1. Together, the results demonstrate a dual effect of ACTH on cell cycle progress, a cAMP-independent growth-promoting effect early in G1 possibly mediated by mitogen-activated protein kinase and c-FOS, and a cAMP-dependent inhibitory effect at mid-G1. It is suggested that the growth-inhibitory effect of ACTH at mid-G1 represents an ACTH-regulated check point that limits cell cycle progression.
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PMID:Unmasking a growth-promoting effect of the adrenocorticotropic hormone in Y1 mouse adrenocortical tumor cells. 936 63

Starvation induces a decrease in circulating leptin levels and activation of the hypothalamus-pituitary-adrenal (HPA) axis. Leptin inhibits the HPA axis in unfed rodents or genetically leptin-deficient ob/ob mice, whereas it stimulates corticotropin-releasing hormone (CRH) gene expression in the paraventricular nucleus (PVN). However, the interactions between leptin, CRH and the HPA axis are poorly understood and are likely to be complex. We recently demonstrated that central leptin administration caused increases in plasma arginine-vasopressin (AVP) and AVP gene expression of the PVN in nonstressful rats. AVP stimulates the release of adrenocorticotropic hormone (ACTH), but it also potentiates the action of CRH on ACTH release. In this study, we investigated the effects of leptin on plasma ACTH and corticosterone levels, CRH mRNA of the PVN and proopiomelanocortin (POMC) mRNA of the pituitary in nonstrained rats. Intracerebroventricularly administered leptin caused increases in plasma ACTH and corticosterone levels in dose-dependent manners. In Northern blot analyses, the leptin injection induced significant increases in the expression of CRH mRNA in the PVN and POMC mRNA in the pituitary. The increased plasma ACTH and corticosterone levels by leptin were attenuated with intracerebroventricular pretreatment of a V(1a) receptor antagonist (OPC-21268) or a V(1a)/V(1b) receptor antagonist (dP[Tyr(Me)(2)]AVP), but not with that of a V(2) receptor antagonist (OPC-31260). The leptin-induced CRH mRNA expression in the PVN and POMC mRNA expression in the pituitary were also reduced by the pretreatment with OPC-21268 and dP[Tyr(Me)(2)]AVP. These results suggest that intracerebroventricular leptin administration activates the HPA axis by AVP receptor activation through V(1a) receptors in the PVN which in turn activates CRH neurons to drive ACTH and corticosterone secretion in concert with AVP in nonstrained rats.
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PMID:Centrally administered murine-leptin stimulates the hypothalamus-pituitary- adrenal axis through arginine-vasopressin. 1087 98

The glycogen body (GB) is in the dorsal area of the lumbosacral spinal cord in birds and is composed of uniform cells characterized by high glycogen storage. The glycogen of GB cells remains unchanged in vivo by the effects of a variety of hormones such as insulin, glucagon, adrenocorticotropic hormone and by physiological conditions such as starvation. In order to investigate the latent functionability of GB cells, we observed morphological changes of glycogen body cells in a co-culture system with cerebellar neurons by light and transmission electron microscopy. Cultured GB cells were labeled with 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI). The cultured neurons derived from cerebellum were co-cultured with the labeled GB cells. Under the co-culture with neurons, 2 types of GB cells were detected. One was conventional with numerous glycogen deposits in the cytoplasm and tended to make clusters. The other type of GB cells singly extended the processes attaching to the neuronal body and axons. In the axons in contact with GB cell processes, small vesicles appearing as synaptic vesicles were observed. These observations suggested that some GB cells can differentiate to an average astrocyte. The GB cells were assumed to involve the synapse formation or maturing as astrocytes in the CNS.
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PMID:Interaction between glycogen body cell and neuron: examination in co-culture system. 1708 87