Animal Models of Obesity 1979
DOI: 10.1007/978-1-349-04201-2_10
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Lipogenesis and hormone resistance in liver and adipose tissue of genetically obese mice

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1979
1979
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Cited by 2 publications
(3 citation statements)
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“…Increased liver weight is also noted in rodents whose obesity is due to a single gene mutation (Hems, 1979). The increased weight of liver and kidneys in the Fat line may have been a result of increased food intake because these organs represent important sites of metabolism and waste excretion.…”
Section: Discussionmentioning
confidence: 99%
“…Increased liver weight is also noted in rodents whose obesity is due to a single gene mutation (Hems, 1979). The increased weight of liver and kidneys in the Fat line may have been a result of increased food intake because these organs represent important sites of metabolism and waste excretion.…”
Section: Discussionmentioning
confidence: 99%
“…Stimulation of phosphatidylinositol turnover (e.g. by vasopressin: Kirk, Verrinder & Hems, 1977, 1979 could be implicated in the control of CaZ+ distribution. All the above-mentioned hormones can inhibit net glycogen synthesis.…”
Section: Hormonal Stimulation Of Catabolism In the Normal Livermentioning
confidence: 99%
“…This impairment is likely to reflect closely the inborn error in these animals, for three reasons: (1) it is not reversible by relatively severe food privation; (2) a lesion in the inhibitory control of fatty acid synthesis would be of direct pathogenic importance, as obesity is by definition a state in which there is excess deposition of fat; (3) in intact obese mice the increase in fatty acid synthesis is intractable to starvation (Hems, Rath & Verrinder, 1975b) as are other alterations in lipid metabolism (Hems, 1979). Such irreversibility suggests thet the lesion in obese mice could reside in the control properties of lipid metabolism.…”
Section: Resistance To Hormonal Control Of Hepatic Catabolism In Obesitymentioning
confidence: 99%