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)

The last third of pregnancy in sheep and goats is characterized by a considerable reduction in the volume of the rumen. When the animal is carrying more than one fetus there is thus a latent ketosis caused by starvation. A discrete hypoglycemia is in close correlation to this. If other special factors like increasing age of the pregnant animal, chronic liver disease, unbalanced nutrition containing too little carbohydrates are also present, the latent starvation ketosis can give rise to an acute gestation ketosis. The clinical picture is described in detail and contrasted with the gestation hypocalcemia. Furthermore, the parameters relevant to laboratory diagnosis will be discussed.
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PMID:[The significance of pregnancy-induced ketonuria in sheep and goats]. 219 Mar 54

To determine risk factors for the development and clinical characteristics of hypoglycemia in patients with sepsis, a case-control study was performed in 52 case-patients who developed spontaneous hypoglycemia (plasma glucose < 50 mg/dl) during episodes of sepsis compared with 49 nondiabetic, control-patients who had sepsis as an immediate cause of death and did not develop hypoglycemia. The presence or absence of potential risk factors for the development of hypoglycemia which consisted of the state of starvation, malnutrition, renal insufficiency, acute or chronic liver disease and malignancy were evaluated in both groups as well as the clinical characteristics of hypoglycemia. The mean of the lowest plasma glucose levels in hypoglycemic patients was 23.4 +/- 14.9 (SD) mg/dl (range 3-47). One-third of patients were found having hypoglycemia since the time of arrival to the hospital. About 90 per cent had septic shock at the time of hypoglycemia. The mortality rate was 90 per cent; 80 per cent died within 48 hours after the first episode of hypoglycemia. Among those risk factors, starvation and liver disease were independently associated with the development of hypoglycemia with odd ratios of 6.38 (95% confidence interval 1.95-20.86; P = 0.002), and 3.59 (95% confidence interval 1.09-11.81; P = 0.035), respectively. In conclusion, hypoglycemia in patients with sepsis was associated with a grave prognosis. The risk of developing hypoglycemia increased significantly in patients who had been fasted for more than 24 hours or had acute or chronic liver disease at the time of sepsis.
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PMID:Hypoglycemia in sepsis: risk factors and clinical characteristics. 947 Mar 28

Man ingests food to mitigate hunger (mediated by physiological and biochemical signals), satisfy appetite (subjective sensation) and because of psychosocial reasons. Satiation biomarkers (stop feeding) are gastric distention and hormones (CCK, GLP-1) and satiety biomarkers (induce feeding) are food-induced thermogenesis, body temperature, glycaemia and also hormones (insulin, leptin and ghrelin). Oxidative metabolism/body composition, tryptophan/serotonin and proinflammatory cytokines are also implicated on hunger physiology. At the present time, ghrelin is the only known circulating orexigenic with potential on hunger/body weight regulation. It is a neuropeptide (endogenous ligand for the GH secretagogue) recently isolated from the oxyntic mucosa and synthesized mainly in the stomach. Its blood concentration depends on diet, hyperglucemia and adiposity/leptin. It is secreted 1-2 hours preprandially and its concentration decreases drastically during the postprandium. Ghrelin acts on the lateral hypothalamus and theoretically inhibits proinflammatory cytokine secretion and antagonizes leptin. Ghrelin physiologically increases food intake and stimulates adipogenesis, gastrointestinal motility and gastric acid secretion, and has other hormonal and cardiovascular functions. Ghrelin blood concentration is reduced in massive obesity, non-alcoholic steatohepatitis, polycystic ovary syndrome, acromegaly, hypogonadism, ageing, short bowel syndrome and rheumatoid arthritis; and increased in primary or secondary anorexia, starvation, chronic liver disease and celiac disease. Cerebral and peritoneal ghrelin administration (rats) and systemic administration (rats and healthy volunteers, cancer patients or patients on peritoneal dialysis) promotes food consumption and increases adiposity, of utmost importance in the treatment of patients with anorexia.
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PMID:[Ghrelin: beyond hunger regulation]. 1705 87

Although undernutrition and starvation continue to affect a substantial portion of the world's population, billions of people in both developed and developing countries are affected by the opposite problem: consumption of calories that exceed their daily energy expenditure, a condition of overnutrition. The body's response to a positive net energy balance is to store energy, predominantly as triglyceride molecules, in the subcutaneous and visceral fat compartments that expand and ultimately manifest in obesity. The body's fat depot, however, does not have an infinite capacity to store and expand, and at set points, which differ from individual to individual and are also influenced by ethnicity, energy substrates 'spill over', resulting in 'ectopic' fat storage in tissues and organs that are not typically major fat storage depots in lean individuals. A complex web of nutrient overload, chronic inflammation, hormonal action, mitochondrial dysfunction and insulin resistance, to mention some of the factors involved, results in devastating metabolic abnormalities that have far reaching implications for health and disease, leading ultimately to some of the most common chronic diseases of our time; i.e., diabetes mellitus, cancer, chronic liver disease and atherosclerosis. Given the complexity and wide-ranging manifestations of overnutrition (also referred to here as insulin resistant states), we will highlight a specific aspect of the condition, that of dyslipidemia. This review will draw mainly on knowledge acquired from whole body, integrative physiology research in animals and humans affected by overnutrition, and will demonstrate how these types of studies can shed light on our understanding of the pathophysiology of the typical dyslipidemia of obesity, insulin resistance and type 2 diabetes.
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PMID:Devastating metabolic consequences of a life of plenty: focus on the dyslipidemia of overnutrition. 2408 28

Real euglycemic diabetic ketoacidosis [DKA; blood glucose <200 mg/dL (11.1 mmol/L)] is rare, and long-lasting starvation conditions due to intervening diseases in type 1 diabetes mellitus patients may also cause it. Euglycemic DKA is also reported in insulin-dependent diabetics with depression, alcoholics, glycogen storage diseases, and chronic liver disease apart from pregnant cases. This case report is presented to emphasize the importance of evaluation of acid-base state, urine glucose, and ketone values at the application in all newly diagnosed type 1 diabetic patients with normal glucose levels by defining euglycemic DKA that resulted from long-lasting starvation during Ramadan fasting in a newly diagnosed 14-year-old male patient.
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PMID:Diabetic euglycemic ketoacidosis in newly diagnosed type 1 diabetes mellitus during Ramadan fasting. 2542 70

Decrease in blood concentration of branched-chain amino acids, especially leucine, is known to promote liver carcinogenesis in patients with chronic liver disease, but the mechanism is unclear. We herein established hepatocellular carcinoma (HCC) cells knocked out for DEPDC5 by using the CRISPR/Cas9 system, and elucidated that cell viability of the DEPDC5 knockout (DEPDC5-KO) cells was higher than that of the DEPDC5 wild-type (DEPDC5-WT) under leucine starvation. Considering that autophagy deficiency might be involved in acquired resistance to leucine deprivation, we observed reduction of LC3-II followed by accumulation of p62 in the DEPDC5-KO, which induced reactive oxygen species (ROS) tolerance. DEPDC5 overexpression suppressed cell proliferation and tumorigenicity in immunocompromised mice, and triggered p62 degradation with increased ROS susceptibility. In clinical specimens of HCC patients, decreased expression of DEPDC5 was positively correlated with p62 overexpression, and the progression-free (PFS) and overall survival (OS) were worse in the DEPDC5-negative cases than in the DEPDC5-positive. Moreover, multivariate analysis demonstrated DEPDC5 was an independent prognostic factor for both PFS and OS. Thus, DEPDC5 inactivation enhanced ROS resistance in HCC under the leucine-depleted conditions of chronic liver disease, contributing to poor patient outcome. It could be a potential target for cancer therapy with oxidative stress control.
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PMID:DEPDC5 deficiency contributes to resistance to leucine starvation via p62 accumulation in hepatocellular carcinoma. 2931

Alcoholic liver disease (ALD) is one of the major causes of chronic liver disease worldwide. Currently, no successful treatments are available for ALD. The pathogenesis of ALD is characterized as simple steatosis, fibrosis, cirrhosis, alcoholic hepatitis (AH), and eventually hepatocellular carcinoma (HCC). Autophagy is a highly conserved intracellular catabolic process, which aims at recycling cellular components and removing damaged organelles in response to starvation and stresses. Therefore, autophagy is considered as an important cellular adaptive and survival mechanism under various pathophysiological conditions. Recent studies from our lab and others suggest that chronic alcohol consumption may impair autophagy and contribute to the pathogenesis of ALD. In this chapter, we summarize recent progress on the role and mechanisms of autophagy in the development of ALD. Understanding the roles of autophagy in ALD may offer novel therapeutic avenues against ALD by targeting these pathways.
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PMID:Role and mechanisms of autophagy in alcohol-induced liver injury. 3130 84

Sarcopenia, a condition of low muscle mass, quality and strength, is commonly found in cirrhotic patients and is associated with adverse clinical outcomes including: reduction in quality of life, increased mortality and post-transplant complications. In chronic liver disease (CLD) it is most commonly defined through the measurement of the skeletal muscle index of the third lumbar spine. A major contributor to sarcopenia in CLD is the imbalance in muscle protein turnover, which likely occurs due to a decrease in muscle protein synthesis and an elevation in muscle protein breakdown. This imbalance is assumed to arise due to a number of factors including: accelerated starvation, hyperammonemia, amino acid deprivation, chronic inflammation, excessive alcohol intake and physical inactivity. In particular, hyperammonemia is a key mediator of the liver-gut axis and is known to contribute to mitochondrial dysfunction and an increase in myostatin expression. Currently, the use of late-evening snacks, branched-chain amino acid supplementation and physical activity have been proposed to help the management and treatment of sarcopenia. However, little evidence exists to comprehensively support their use in clinical settings. A number of new, pharmacological strategies, including myostatin inhibition and the nutraceutical Urolithin A have recently been proposed to treat age-related sarcopenia, and may also be of use in CLD. This review highlights the potential molecular mechanisms contributing to sarcopenia in CLD alongside a discussion of existing and potential new treatment strategies.
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PMID:Sarcopenia in Chronic Liver Disease: Mechanisms and Countermeasures. 3323 53