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

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 interaction between genetic constitution and in utero environment determines fetal growth and development and influences the susceptibility to certain disorders in adulthood. Data from both animal and human studies indicate that prenatal and early postnatal malnutrition can program the hypothalamus-pituitary-adrenal axis (HPA axis), altering neuroendocrine response to stressors throughout lifetime. Impaired uteroplacental perfusion results in fetal growth restriction (FGR). In FGR there is evidence of chronic hypoxemia and alterations in metabolic, endocrine, and hematological parameters, compatible with starvation. Furthermore, FGR is associated with increased perinatal mortality and in the survivors there is increased susceptibility to diabetes and cardiovascular disease in adulthood. There is evidence that early postnatal growth acceleration, which would normally be considered desirable, may exacerbate metabolic dysfunction in later life.
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PMID:Fetal growth restriction and postnatal development. 1730 57

Glucocorticoids (GCs) are the final effector products of a neuroendocrine HPA/HPI axis governing energy balance and stress response in vertebrates. From a physiological point of view, basal GC levels are essential for intermediary metabolism and participate in the development and homeostasis of a wide range of body tissues, including the skeleton. Numerous mammalian studies have demonstrated that GC hormones exert a positive role during bone modeling and remodeling as they promote osteoblastogenesis to maintain the bone architecture. Although the pharmacological effect of the so-called stress hormones has been widely reported, the role of endogenous GCs on bone mineral metabolism as result of the endocrine stress response has been largely overlooked across vertebrates. In addition, stress responses are variable depending on the stressor (e.g., starvation, predation, and environmental change), life cycle events (e.g., migration and aging), and differ among vertebrate lineages, which react differently according to their biological, social and cognitive complexity (e.g., mineral demands, physical, and psychological stress). This review intends to summarize the endogenous GCs action on bone metabolism of mammals and fish under a variety of challenging circumstances. Particular emphasis will be given to the regulatory loop between GCs and the parathyroid hormone (PTH) family peptides, and other key regulators of mineral homeostasis and bone remodeling in vertebrates.
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PMID:Stress, Glucocorticoids and Bone: A Review From Mammals and Fish. 3025 Apr 53

The residue of simazine herbicide in the environment is known as one of pollutant stress for lizards by crippling its fitness on direct toxic effects and indirect food shortage via the food chain effects. Both stressors were considered in our experiment in the simazine exposure and food availability to lizards (Eremias argus). The results revealed that starvation significantly reduced the lizard's energy reserve and native immune function, while the accumulation of simazine in the liver was significantly increased. Simazine caused oxidative stress in the liver of lizards, but oxidative damage only occurred in the starved lizards. Simazine also changed the energy reserves, native immune function and detoxification of well-fed lizards, while the starved lizards showed different sensitivity to simazine. Simazine or starvation treatment independently activated the lizard HPA axis, but co-treatment caused the HPA axis inhibition. Besides, according to the variations on amino acid neurotransmitters, corticosterone hormone and thermoregulatory behavior, we inferred that lizards in threatens take the appropriate strategy on energy investment and allocation through neural, endocrine and behavioral pathways to maximize benefits in dilemma. Energy allocation was necessary, while suppression on any physiological process comes at a cost that is detrimental to long-term individual fitness.
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PMID:Effects of simazine and food deprivation chronic stress on energy allocation among the costly physiological processes of male lizards (Eremias argus). 3330 94