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

The present study was undertaken to determine whether alterations in ketone body utilization and hepatic production, independent of the FFA load, were also involved in the development of fasting ketosis. Plasma Beta-OH butyric acid (Beta-OHB) increased to 2.5-4.5 mM and plasma FFA to 1,000-1,400 muEq/L. in normal weight individuals after five to seven days' starvation and in obese subjects after ten to fourteen days' fasting. Acute elevations fo the plasma FFA greater than 1,500 muEq/L. for sixty minutes in fed normal weight and obese subjects with a fat meal-heparin regimen resulted in peak elevations of plasma Beta-OHB (0.25-0.45mM), only 10 percent of that seen during fasting. When plasma FFA were lowered acutely during fasting with the antilipolytic agent Pyrazole to control levels (400-600 muEq/L.), plasma Beta-OHB decreased 35 plus or minus 5 per cent. Comparable lowering of plasma FFA in normal weight or obese starved subjects given dexamethasone to maintain elevated fasting plasma insulin levels resulted in an 87 plus or minus 3 per cent decrease in plasma Beta-OHB. Similar studies in obese fasted subjects pretreated with an intravenous infusion of insulin (1.0 U/hr. for eight hours) before receiving Pyrazole resulted in a 65 plus or minus 5 per cent decrease in plasma Beta-OHB. Plasma Beta-OHB half-life, determined after injections of 12 gm. Beta-OHB, increased significantly during fasting (110 plus or minus 15 minutes) and was decreased when the fasting subjects were maintained on dexamethasone (65 plus or minus 7 minutes). These studies indicate that accelerated hepatic ketogenesis during starvation is a result of both enhanced activity of the enzymatic system(s) involved in ketone body production as well as an increased FFA load. The increase in plasma Beta-OHB during fasting reflects not only an accelerated rate of hepatic ketogenesis but also an impairment of peripheral utilization, both processes apparently being sensitive to insulin. Diabetes 24:10-16, January, 1975.
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PMID:Physiologic mechanisms in the development of starvation ketosis in man. 112 May 41

Nutrition of colonic epithelial cells is mainly from short chain fatty acids (SCFAs) produced by bacterial fermentation in the colonic lumen. n-Butyrate contributes more carbon of oxidation to epithelial cells than glucose or glutamine from the vasculature. Incomplete starvation of colonic epithelial cells through lack of luminal SCFAs leads, in the short term, to mucosal hypoplasia with either diminished absorption or diarrhea. A chronic lack of SCFAs or complete organ starvation in conjunction with other factors leads to nutritional colitis, either "diversion colitis" or "starvation colitis." Whether predominantly diarrhea or colitis develops in mucosal malnutrition appears to depend upon the severity and duration of starvation. Ulcerative colitis may be classified as a nutritional colitis in that colonic epithelial cells are unable to utilize SCFAs reflecting epithelial starvation despite abundant SCFAs.
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PMID:The starved colon--diminished mucosal nutrition, diminished absorption, and colitis. 220 75

The effect of cell cycle on Rb+ (K+) fluxes was studied in NIH 3T3 mouse fibroblasts. Serum starvation or isoleucine deprivation resulted in cell arrest at an early G1/G0 phase, accompanied by a marked decrease in both ouabain-sensitive and ouabain-resistant Rb+ influx. On the other hand, cells arrested at late G1/G0 phase by hydroxyurea treatment have high ouabain-sensitive and ouabain-resistant Rb+ influx. Butyric acid treatment resulted in cell arrest at an early G1/G0 phase, but in contrast to serum or isoleucine starvation did not decrease Rb+ influxes. It is thus shown that quiescent cells may have Rb+ influx rates as high as that of logarithmically growing cells. The results are consistent with the hypothesis that an increased ion permeability of the cell is initiated at a critical stage in G1/G0 phase, and that butyric acid may arrest the cell beyond that stage.
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PMID:Rb+ influxes differentiate between growth arrest of cells by different agents. 631 30

The effect of starvation for five days on blood levels of various hormones and metabolites was studied in seven steers. There was a significant decrease (P less than 0.05) in thyroxine (free and total), 3,5,3'-triiodothyronine (free and total), immunoreactive insulin, propionic acid, butyric acid and glucose, 3,3',5'-triiodothyronine and alpha-aminoacid-N levels did not change. Free fatty acids, beta-hydroxybutyrate, acetoacetate, urea, isobutyrate, alpha-methylbutyrate and isovalerate, total protein and albumin significantly (P less than 0.05) increased.
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PMID:Metabolic effects of fasting in steers. 731 12

The intestinal metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was investigated in male and female Sprague-Dawley (SD) rats and male F344 rats, using isolated perfused intestinal segments. [1(-14)C]-NNK at 1 microM was metabolized by alpha-hydroxylation, pyridine N-oxidation and carbonyl reduction. Jejunal segments from control female rats metabolized 26.2% of the NNK during transepithelial transfer to 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL, 12.2%), 4-(methylnitrosamino)-1-3-pyridyl-N-oxide)-1-butanone (NNK-N-oxide, 7.7%), 4-oxo-4-(3-pyridyl)-butanol (KAlc, 2.7%), 4-(methylnitrosamino)-1-(3-pyridyl-N-oxide)-1-butanol (NNAL-N-oxide, 1.8%), 4-oxo-4-(3-pyridyl)butyric acid (KA, 1.1%) and 4-hydroxy-4-(3-pyridyl)butyric acid (HA, 0.7%). Ileal segments metabolized 20.8% of the NNK during absorption, with no difference in metabolite distribution as compared to jejunal segments. In control male SD and F344 rats, jejunal presystemic metabolism was 2.3-fold higher (56.4% and 60.8% respectively), mainly because of a 4-fold increase in NNAL formation (44.1% and 48.5%)> total NNK metabolism was also induced in female rats by starvation (84.4% metabolites), acetone (89.3%), phenobarbital PB, 75.3%) and Clophen A50 (61%). PB and Clophen A50 induced N-oxidation to 38.9% (4 x) and 27.8% (3 x), and to a lesser extent NNAL formation and alpha-hydroxylation (2 x), Starvation mainly increased N-oxidation with a time-dependent increase from 1 day to 3 days of starvation (4 x and 8 x versus controls), whereas alpha-hydroxylation and NNAL formation was elevated only after 1 day starvation. Acetone pretreatment (3 days) stimulated all three pathways (NNAL 2 x, N-oxidation 4 x, alpha-hydroxylation 4 x). In male F344 rats, starvation and acetone induced N-oxidation (5 x and 7 x) and alpha-hydroxylation (3 x and 5 x), and decreased NNAL formation by 40%, probably due to substrate competition or further metabolism of NNAL. In acetone-induced female SD rats, NNK metabolism was inhibited by in vivo pretreatment with phenethylisothiocyanate (PEITC) or in vitro addition of 1% ethanol to the perfusate. Both inhibition experiments reduced total metabolism by 20%; N-oxidation and alpha-dhyroxylation were reduced to values found in control rats, whereas NNAL formation increased from 31% to 51%.Inhibition of NNK metabolism by PEITC im male F344 rats was less pronounced compared to female SD rats; again a decrease in alpha-hydroxylation (6.7% to 3.3%) and N-oxidation (73.6% to 35.3) was accompanied by increased NNAL formation (9.8% to 41.0%).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Intestinal metabolism of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone in rats: Sex difference, inducibility and inhibition by phenethylisothiocyanate. 763 97

Isolated colonocytes have more capacity for the oxidation of isobutyrate and alpha-ketoisovalerate than isolated enterocytes. Both enterocytes and colonocytes express high levels of 3-hydroxyisobutyryl-CoA hydrolase, an enzyme activity important in maintaining low intracellular concentrations of methacrylyl-CoA, a common, potentially toxic intermediate in the catabolic pathways of these compounds. In spite of comparable 3-hydroxyisobutyryl-CoA hydrolase activities in both cell types, and much greater amounts of 3-hydroxyisobutyrate dehydrogenase in colonocytes than in enterocytes, only the colonocytes produced 3-hydroxyisobutyrate as an endproduct of alpha-ketoisovalerate and isobutyrate catabolism. Butyrate very effectively inhibits isobutyrate catabolism by colonocytes, most likely by competitively inhibiting activation of isobutyrate to its CoA ester. Oleate also inhibits isobutyrate catabolism, but at a site more distal than butyrate. Starvation of rats for 72 h decreased the capacity of colonocytes for butyrate but not isobutyrate catabolism. We conclude that isobutyrate could function as a carbon source for energy and anapleurosis in colonocytes under conditions of defective butyrate oxidation or low butyrate availability.
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PMID:Catabolism of isobutyrate by colonocytes. 861 13

Pseudomonas aeruginosa PAO1 used a broad range of alkanesulfonic acids as sole sulfur source for growth, with molar growth yields of 2.2 to 2.9 kg protein per mol sulfur. 4-Phenylbutane-1-sulfonate was desulfonated in vivo to yield 4-phenyl-1-butyric acid quantitatively as the sole product, suggesting that the desulfonation mechanism is the same as when alkanesulfonates serve as a carbon source for growth. This contrasts with aromatic sulfonate utilization in other organisms, where different desulfonation reactions are used to provide carbon and sulfur. Desulfonation of alkanesulfonates to provide sulfur was repressed by sulfate or thiocyanate, and derepressed in their absence. The alkanesulfonatase system is hence controlled as part of the sulfate starvation-induced stimulon.
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PMID:Desulfonation of aliphatic sulfonates by Pseudomonas aeruginosa PAO. 899 89

The tryptophan (Trp) biosynthetic pathway leads to the production of many secondary metabolites with diverse functions, and its regulation is predicted to respond to the needs for both protein synthesis and secondary metabolism. We have tested the response of the Trp pathway enzymes and three other amino acid biosynthetic enzymes to starvation for aromatic amino acids, branched-chain amino acids, or methionine. The Trp pathway enzymes and cytosolic glutamine synthetase were induced under all of the amino acid starvation test conditions, whereas methionine synthase and acetolactate synthase were not. The mRNAs for two stress-inducible enzymes unrelated to amino acid biosynthesis and accumulation of the indolic phytoalexin camalexin were also induced by amino acid starvation. These results suggest that regulation of the Trp pathway enzymes under amino acid deprivation conditions is largely a stress response to allow for increased biosynthesis of secondary metabolites. Consistent with this hypothesis, treatments with the oxidative stress-inducing herbicide acifluorfen and the abiotic elicitor alpha-amino butyric acid induced responses similar to those induced by the amino acid starvation treatments. The role of salicylic acid in herbicide-mediated Trp and camalexin induction was investigated.
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PMID:Induction of Arabidopsis tryptophan pathway enzymes and camalexin by amino acid starvation, oxidative stress, and an abiotic elicitor. 950 Nov 10

A diet high in fiber is associated with a decreased incidence and growth of colon cancers. Butyrate, a four-carbon short-chain fatty acid product of fiber fermentation within the colon, appears to mediate these salutary effects. We sought to determine the molecular mechanism by which butyrate mediates growth inhibition of colonic cancer cells and thereby to elucidate the molecular link between a high-fiber diet and the arrest of colon carcinogenesis. We show that concomitant with growth arrest, butyrate induces p21 mRNA expression in an immediate-early fashion, through transactivation of a promoter cis-element(s) located within 1.4 kb of the transcriptional start site, independent of p53 binding. Studies using the specific histone hyperacetylating agent, trichostatin A, and histone deacetylase 1 indicate that growth arrest and p21 induction occur through a mechanism involving histone hyperacetylation. We show the critical importance of p21 in butyrate-mediated growth arrest by first confirming that stable overexpression of the p21 gene is able to cause growth arrest in the human colon carcinoma cell line, HT-29. Furthermore, using p21-deleted HCT116 human colon carcinoma cells, we provide convincing evidence that p21 is required for growth arrest to occur in response to histone hyperacetylation, but not for serum starvation nor postconfluent growth. Thus, p21 appears to be a critical effector of butyrate-induced growth arrest in colonic cancer cells, and may be an important molecular link between a high-fiber diet and the prevention of colon carcinogenesis.
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PMID:p21(WAF1) is required for butyrate-mediated growth inhibition of human colon cancer cells. 961 91

This article reviews data that have accumulated since the early 1970s on the role of the dorsomedial hypothalamic nucleus (DMN) in neuroendocrine and autonomic homeostasis. Both the ventromedial hypothalamic nucleus (VMN) and the lateral hypothalamic area (LHA) project to the DMN, which in turn projects to the paraventricular nucleus of the hypothalamus (PVN), thus placing the DMN at an important nodal point of neuroendocrine/autonomic circuitries. The DMN is composed of cells and fibers containing neuropeptide Y (NPY), and the nutritional status (starvation-refeeding) is reflected in NPY levels of both VMN and DMN in Sprague-Dawley, Zucker (fa/fa), and corpulent rats (cp/cp JCR:LA). The DMN is involved in the final common pathway of corticotrophin-releasing hormone (CRH) secretion by the PVN, sympathetic nervous system outflow to the adrenal gland, and brown adipose tissue (BAT) thermogenesis. The DMN is also part of a "fear circuitry" regulating cardiovascular responses to stress such as myocardial blood flow and the tachycardia associated with the defense reaction. This appears to be mediated by a gamma amino butyric acid (GABA) mechanism. Although exhibiting reduced ponderal and linear growth and hypophagia and hypodipsia, the rat with DMN lesions (DMNL rat) has normal body composition, anabolic hormone levels, and intermediary metabolism, and it responds normally to numerous endocrine, nutritional, intra- and extracellular thirst and body weight-regulatory challenges. The DMNL rat shows normal efficiency of food utilization, but shows an attenuated response to the feeding-stimulatory effect of insulin. The only other lesion-induced abnormalities are hyperprolactinemia and a disrupted circadian corticosterone rhythm. The hyperprolactinemia in DMNL rats appears to be related to an attenuation of dopamine (DA). Rats with DMNL are capable of mating and can bear offspring, but there is a dramatic effect on litter size and other litter parameters that only improves when one parent is a DMNL rat. Antiaging effects produced by DMNL are evident in the prevention of age-associated microalbuminuria and kidney lesions, as well as, in prevention of the age-related decline in circulating insulin-like growth factor I (IGF-I). Recent evidence suggests that DMN, together with the VMN and the arcuate nucleus (ARC) of the hypothalamus, may be part of the circuitry that is responsive to the feedback signal from adipose tissue by the hormone leptin. The above findings and others suggest that the DMN plays a diverse role in physiological regulatory processes.
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PMID:The dorsomedial hypothalamic nucleus revisited: 1998 update. 971 72


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