The contribution of protein turnover to energy balance in the genetically obese (ob/ob) mouse
The contribution of protein turnover to energy balance in the genetically obese (ob/ob) mouse
The fate of 100 µCi of 2-[3 H] glutarnic acid injected intraperitoneally into lean (Ob/+) and obese (ob/ob) mice was investigated. [3 H] was rapidly lost from glutamate and incorporated into water. By 10h the amino acid pool was unlabelled and < 1% of [3H] had become incorporated into protein. Analysis of tissue protein (liver, intestine and kidney) showed that only glutamate was significantly labelled. The decay of specific and total activity of the tissue proteinwas therefore taken, respectively, as an accurate representation of protein synthesis and catabolism. A comparative study using lean and obese mice over arange of dietary energy intakes (DEI) was undertaken(Lean: 45.2 - 107.6 kJ/d; obese: 33.6 - 126. 1 kJ/d). Protein turnover (mg/d) was measured in liver, intestine and kidney. In lean mice, liver protein turnover showed a sigmoidal relationship with DEI, and both kidney and intestinal protein turnover were elevated at the highest DEI (obtained by cold adaptation). In marked contrast, protein turnover in the liver,intestine and kidney of obese mice was not affected by DEI. A second comparative study on lean and obese mice was undertaken, in which in vitro incorporation of [3H] leucine into liver protein and hepatic RNA P /mg protein was measured. Three experimental conditions were investigated-(I) Cold stress: fed mice (2) Cold stress: fasted mice; and (3) Feeding following 48h fast. In all conditions [3 H] leucine incorporation was enhanced in lean mice compared to theirobese siblings. Marked differences were observed in RNA / P mg protein between lean and obese mice. In conclusion the data presented in this thesis supports the hypothesis that protein turnover is a component of dietary induced thermogenesis and non shivering thermogenesis. The possibility that a defect in translation in the (ob/ob) mice may be central to the aeteology of their obesity is discussed.
University of Southampton
Miller, Bevis Graham
931a771a-747e-48e3-8f97-b9c510dd0b7f
1978
Miller, Bevis Graham
931a771a-747e-48e3-8f97-b9c510dd0b7f
Miller, Bevis Graham
(1978)
The contribution of protein turnover to energy balance in the genetically obese (ob/ob) mouse.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
The fate of 100 µCi of 2-[3 H] glutarnic acid injected intraperitoneally into lean (Ob/+) and obese (ob/ob) mice was investigated. [3 H] was rapidly lost from glutamate and incorporated into water. By 10h the amino acid pool was unlabelled and < 1% of [3H] had become incorporated into protein. Analysis of tissue protein (liver, intestine and kidney) showed that only glutamate was significantly labelled. The decay of specific and total activity of the tissue proteinwas therefore taken, respectively, as an accurate representation of protein synthesis and catabolism. A comparative study using lean and obese mice over arange of dietary energy intakes (DEI) was undertaken(Lean: 45.2 - 107.6 kJ/d; obese: 33.6 - 126. 1 kJ/d). Protein turnover (mg/d) was measured in liver, intestine and kidney. In lean mice, liver protein turnover showed a sigmoidal relationship with DEI, and both kidney and intestinal protein turnover were elevated at the highest DEI (obtained by cold adaptation). In marked contrast, protein turnover in the liver,intestine and kidney of obese mice was not affected by DEI. A second comparative study on lean and obese mice was undertaken, in which in vitro incorporation of [3H] leucine into liver protein and hepatic RNA P /mg protein was measured. Three experimental conditions were investigated-(I) Cold stress: fed mice (2) Cold stress: fasted mice; and (3) Feeding following 48h fast. In all conditions [3 H] leucine incorporation was enhanced in lean mice compared to theirobese siblings. Marked differences were observed in RNA / P mg protein between lean and obese mice. In conclusion the data presented in this thesis supports the hypothesis that protein turnover is a component of dietary induced thermogenesis and non shivering thermogenesis. The possibility that a defect in translation in the (ob/ob) mice may be central to the aeteology of their obesity is discussed.
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Published date: 1978
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Local EPrints ID: 467225
URI: http://eprints.soton.ac.uk/id/eprint/467225
PURE UUID: 31403b81-3a8a-4387-8b8e-a3be71807a7a
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Date deposited: 05 Jul 2022 08:16
Last modified: 23 Jul 2022 01:17
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Author:
Bevis Graham Miller
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