Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two sets of observations are reported as illustrations of problems encountered in behavioral toxicology. First, in an attempt to determine the contribution of methylmercury-induced ataxia to behavioral changes observed on the fixed-consecutive-number schedule, some ancillary control experiments were undertaken. Neither pharmacologically-produced incoordination (ethanol) nor mechanically-produced incoordination (foot taping) led to behavioral changes similar to those seen after exposure to methylmercury. Second, total crop impaction in a pigeon that died during a behavioral experiment on lead suggested some further work. Lead-induced crop stasis in pigeons was measured by x-raying the passage of force-fed stainless steel ball bearings through the crop. This retardation of motility reliably preceded signs of overt toxicity. These results suggest that the behavioral changes in the pigeon noted by us and reported by other investigators cannot be attributed to CNS dysfunction alone, but more likely arise from starvation, or from combined CNS damage and starvation. In addition, these results demonstrate that the appearance of behavioral effects prior to overt toxicity does not necessarily reflect CNS damage.
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PMID:Some problems in interpreting the behavioral effects of lead and methylmercury. 29 71

Diagnosis and treatment of hypoglycemia is an actual problem because glucose is the principal source of energy for central nervous system except permanent starvation when the ketone bodies are used by the central nervous system for energy. Glucose homeostasis depends on primary glucoregulatory organs--pancreas, liver, adrenal glands, and hypophysis. Insulin, glucagon, cathecholamines, cortisol, and growth hormone take part in this interaction. Hypoglycemia can develop if there are disorders of glucoregulatory organs resulting in imbalance of normal glucose homeostasis. Hypoglycemia presents with autonomic symptoms--hunger, palpitations, tremor, sweating--and with neuroglycopenic symptoms--confusion, drowsiness, odd behavior, speech difficulties, incoordination. None of these symptoms is specific just to hypoglycemia. Frequently hypoglycemia has to be differentiated with neurologic, psychiatric, and cardiovascular disorders. In this article the causes, symptoms, diagnosis, and treatment of hypoglycemia are reviewed.
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PMID:[Causes, diagnosis, and treatment of hypoglycemia]. 1709 Sep 87

Macroautophagy, commonly referred to as autophagy, is a protein degradation pathway that occurs constitutively in cells, but can also be induced by stressors such as nutrient starvation or protein aggregation. Autophagy has been implicated in multiple disease mechanisms including neurodegeneration and cancer, with both tumor suppressive and oncogenic roles. Uncoordinated 51-like kinase 1 (ULK1) is a critical autophagy protein near the apex of the hierarchal regulatory pathway that receives signals from the master nutrient sensors MTOR and AMP-activated protein kinase (AMPK). In mammals, ULK1 has a close homolog, ULK2, although their functional distinctions have been unclear. Here, we show that ULK1 and ULK2 both function to support autophagy activation following nutrient starvation. Increased autophagy following amino acid or glucose starvation was disrupted only upon combined loss of ULK1 and ULK2 in mouse embryonic fibroblasts. Generation of PtdIns3P and recruitment of WIPI2 or ZFYVE1/DFCP1 to the phagophore following amino acid starvation was blocked by combined Ulk1/2 double knockout. Autophagy activation following glucose starvation did not involve recruitment of either WIPI1 or WIPI2 to forming autophagosomes. Consistent with a PtdIns3P-independent mechanism, glucose-dependent autophagy was resistant to wortmannin. Our findings support functional redundancy between ULK1 and ULK2 for nutrient-dependent activation of autophagy and furthermore highlight the differential pathways that respond to amino acid and glucose deprivation.
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PMID:Regulation of nutrient-sensitive autophagy by uncoordinated 51-like kinases 1 and 2. 2329 78