Protective effect of small amounts of glucose on abnormal liver function tests during starvation

Abraira, Carlos; Virupannavar, C.; Nemchausky, Bernard M.

doi:10.1016/0026-0495(80)90037-2

Cited by 10 publications

(3 citation statements)

References 13 publications

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“…Browning et al, 2012). Fasting for 48 h reduced ALP levels in all experimental animals, as has been reported in chow-fed control and CCl4-induced cirrhotic rats (Abraira et al, 1980;Krahenbuhl et al, 1991;Restellini et al, 2013;Fazeli et al, 2015).…”

Section: Discussionsupporting

confidence: 80%

Contrasting Effects of Fasting on Liver-Adipose Axis in Alcohol-Associated and Non-alcoholic Fatty Liver

et al. 2021

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Background: Fatty liver, a major health problem worldwide, is the earliest pathological change in the progression of alcohol-associated (AFL) and non-alcoholic fatty liver disease (NAFL). Though the causes of AFL and NAFL differ, both share similar histological and some common pathophysiological characteristics. In this study, we sought to examine mechanisms responsible for lipid dynamics in liver and adipose tissue in the setting of AFL and NAFL in response to 48 h of fasting.Methods: Male rats were fed Lieber-DeCarli liquid control or alcohol-containing diet (AFL model), chow or high-fat pellet diet (NAFL model). After 6–8 weeks of feeding, half of the rats from each group were fasted for 48 h while the other half remained on their respective diets. Following sacrifice, blood, adipose, and the liver were collected for analysis.Results: Though rats fed AFL and NAFL diets both showed fatty liver, the physiological mechanisms involved in the development of each was different. Here, we show that increased hepatic de novo fatty acid synthesis, increased uptake of adipose-derived free fatty acids, and impaired triglyceride breakdown contribute to the development of AFL. In the case of NAFL, however, increased dietary fatty acid uptake is the major contributor to hepatic steatosis. Likewise, the response to starvation in the two fatty liver disease models also varied. While there was a decrease in hepatic steatosis after fasting in ethanol-fed rats, the control, chow and high-fat diet-fed rats showed higher levels of hepatic steatosis than pair-fed counterparts. This diverse response was a result of increased adipose lipolysis in all experimental groups except fasted ethanol-fed rats.Conclusion: Even though AFL and NAFL are nearly histologically indistinguishable, the physiological mechanisms that cause hepatic fat accumulation are different as are their responses to starvation.

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Section: Discussionsupporting

confidence: 80%

Contrasting Effects of Fasting on Liver-Adipose Axis in Alcohol-Associated and Non-alcoholic Fatty Liver

et al. 2021

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“…Hypophosphataemia occurred despite a restricted oral energy intake, which was well below that required to meet the demands of the basal metabolic rate. Elevated bilirubin concentrations and liver enzymes are a known complication of starving in humans (13)(14)(15)(16) and our subject's results suggest that the observed changes seen may reflect a harmless, perhaps physiological effect of the refeeding process. Elevated levels of vitamin B12 and zinc are probably due to loss from liver and other lean tissues because of tissue catabolism during fasting, or could represent changes in B12 kinetics, transport proteins or enterohepatic circulation (17,18).…”

Section: Discussionmentioning

confidence: 65%

Metabolic and hormonal changes during the refeeding period of prolonged fasting

Korbonits¹,

Blaine²,

Elia³

et al. 2007

eur j endocrinol

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Objective: The discovery of leptin, a hormone primarily involved in adaptation to fasting, led to an increased interest in appetite regulation and appetite-modulating hormones. Here, we present unique data from a case of extreme starvation and refeeding, showing changes in plasma concentrations of appetite-modulating and metabolic hormones as well as biochemical changes, and draw attention to the dangers of the refeeding syndrome. Patients and methods: We studied the refeeding period of a 44-day voluntary fast uncomplicated by underlying disease. Biochemical and hormonal variables were compared with 16 matched subjects such that the BMI range of the controls covered the entire spectrum for the index subject's recovering BMI. Results: Lack of calorie intake with free access to water resulted in 25% loss of body weight. Haemoconcentration was observed and feeding was started with a low sodium, hypocaloric liquid formulation. During early refeeding, marked hypophosphataemia, haemodilution and slight oedema developed. Vitamins B1, B12 and B6 were depleted while serum free fatty acids, ketone bodies and zinc levels were abnormally high; abnormal liver function developed over the first week. The hormonal profile showed low IGF-I and insulin levels, and elevated IGF-binding protein-1 concentrations. Appetite-regulating hormones were either very low (leptin and ghrelin) or showed no marked difference from the control group (peptide YY, agouti-related peptide, a-melanocytestimulating hormone, neuropeptide Y and pro-opiomelanocortin). Appetite was low at the beginning of refeeding and a transient increase in orexin and resistin was observed coincidently with an increase in subjective hunger. Conclusions: Our study illustrates the potential dangers of refeeding and provides a comprehensive insight into the endocrinology of prolonged fasting and the refeeding process.European Journal of Endocrinology 157 157-166

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“…Given the delayed time course of FGF21 production in humans, we hypothesized a functional relevance in the late phases of the starvation response, finding significant associations between FGF21 and both AST (a marker of tissue breakdown) and weight loss in a longitudinal analysis. The induction of AST with fasting has previously been demonstrated in humans; however, interestingly, it was shown that concurrent administration of small doses of oral glucose -insufficient to correct the marked negative calorie balance -reversed the fasting-mediated increase in serum AST levels, while also improving markers of protein catabolism (41). We speculate that each individual has a threshold of weight loss during starvation that, when exceeded, results in tissue stress jci.org Volume 125 Number 12 December 2015…”

Section: Discussionmentioning

confidence: 96%