Feeding Response to Mercaptoacetate in Osborne‐Mendel and S5B/PL Rats

SINGER, LORI K, DAVID A YORK, GEORGE A BRAY. Feeding response to mercaptoacetate in Osborne‐Mendel and S5B/PL Rats. The purpose of this experiment was to determine if Osborne‐Mendel (OM) rats, which are susceptible to dietary‐induced obesity, and S5B/PL (S5B) rats, which are resistant to dietary‐ind...

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Veröffentlicht in:Obesity research 1997-11, Vol.5 (6), p.587-594
Hauptverfasser: Singer, Lori K., York, David A., Bray, George A.
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Sprache:eng
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Zusammenfassung:SINGER, LORI K, DAVID A YORK, GEORGE A BRAY. Feeding response to mercaptoacetate in Osborne‐Mendel and S5B/PL Rats. The purpose of this experiment was to determine if Osborne‐Mendel (OM) rats, which are susceptible to dietary‐induced obesity, and S5B/PL (S5B) rats, which are resistant to dietary‐induced obesity, differ in their feeding responses to mercaptoacetate (MA), which blocks fatty acid oxidation, or 2‐deoxy‐D‐glucose (2DG), which blocks glucose utilization. 2DG (100 mg/kg or 200 mg/ kg) increased food intake in both strains of rats on a high‐fat diet (56% energy from fat). Mercaptoacetate (600 umol/kg) increased food intake in OM but not S5B rats on a high‐fat diet. When maintained on a low‐fat diet (10% energy from fat), MA (400 umol/kg or 600 umol/kg) stimulated food intake in OM rats, whereas S5B rats increased food intake only after the highest dose of MA (600 umol/kg). MA stimulated carbohydrate and protein intake in OM rats maintained on a macro‐nutrient selection diet, whereas S5B rats maintained on this diet did not significantly increase intake of any mac‐ronutrient after MA. These results demonstrate that OM and S5B rats have a similar food intake response to 2DG but a dissimilar response to MA. The variable response to MA in these strains may be due to a difference in peripheral or central signaling systems related to fatty acid oxidation or a difference in metabolic environments between the strains, which in turn affects the feeding response to MA. These studies suggest that a difference in control of fatty acid oxidation may account for the difference in susceptibility to obesity when eating a high‐fat diet.
ISSN:1071-7323
1550-8528
DOI:10.1002/j.1550-8528.1997.tb00580.x