Literature DB >> 371355

Energy metabolism in feasting and fasting.

O E Owen, G A Reichard, M S Patel, G Boden.   

Abstract

During feasting on a balanced carbohydrate, fat, and protein meal resting metabolic rate, body temperature and respiratory quotient all increase. The dietary components are utilized to replenish and augment glycogen and fat stores in the body. Excessive carbohydrate is also converted to lipid in the liver and stored along with the excessive lipids of dietary origin as triglycerides in adipose tissue, the major fuel storage depot. Amino acids in excess of those needed for protein synthesis are preferentially catabolized over glucose and fat for energy production. This occurs because there are no significant storage sites for amino acids or proteins, and the accumulation of nitrogenous compounds is ill tolerated. During fasting, adipose tissue, muscle, liver, and kidneys work in concert to supply, to convert, and to conserve fuels for the body. During the brief postabsorptive period, blood fuel homeostasis is maintained primarily by hepatic glycogenolysis and adipose tissue lipolysis. As fasting progresses, muscle proteolysis supplies glycogenic amino acids for heightened hepatic gluconeogenesis for a short period of time. After about three days of starvation, the metabolic profile is set to conserve protein and to supply greater quantities of alternate fuels. In particular, free fatty acids and ketone bodies are utilized to maintain energy needs. The ability of the kidney to conserve ketone bodies prevents the loss of large quantities of these valuable fuels in the urine. This delicate interplay among liver, muscle, kidney, and adipose tissue maintains blood fuel homeostasis and allows humans to survive caloric deprivation for extended periods.

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Year:  1979        PMID: 371355     DOI: 10.1007/978-1-4757-0734-2_8

Source DB:  PubMed          Journal:  Adv Exp Med Biol        ISSN: 0065-2598            Impact factor:   2.622


  28 in total

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Review 3.  Inflammatory bowel disease and immunonutrition: novel therapeutic approaches through modulation of diet and the gut microbiome.

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4.  The Role of Leptin in Maintaining Plasma Glucose During Starvation.

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5.  Metabolic master regulators: sharing information among multiple systems.

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7.  The SNF1 Kinase Ubiquitin-associated Domain Restrains Its Activation, Activity, and the Yeast Life Span.

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8.  Burst-like control of lipolysis by the sympathetic nervous system in vivo.

Authors:  Katrin Hücking; Marianthe Hamilton-Wessler; Martin Ellmerer; Richard N Bergman
Journal:  J Clin Invest       Date:  2003-01       Impact factor: 14.808

9.  Sarcopenia and a physiologically low respiratory quotient in patients with cirrhosis: a prospective controlled study.

Authors:  Cathy Glass; Peggy Hipskind; Cynthia Tsien; Steven K Malin; Takhar Kasumov; Shetal N Shah; John P Kirwan; Srinivasan Dasarathy
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10.  Fasting adaptation in idiopathic ketotic hypoglycemia: a mismatch between glucose production and demand.

Authors:  Hidde H Huidekoper; Marinus Duran; Marjolein Turkenburg; Mariëtte T Ackermans; Hans P Sauerwein; Frits A Wijburg
Journal:  Eur J Pediatr       Date:  2007-10-13       Impact factor: 3.183

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