The genetically dystrophic line of hamsters (BIO 14.6) has a significantly reduced capacity for nonshivering thermogenesis (NST) when compared with age-matched normal animals. Of those tissues contributing most to NST, three are altered in the dystrophic hamster (brown fat and cardiac and skeletal muscle). This study has used regional blood flows in response to isoproterenol (a potent stimulator of NST) as a measure of the potential contribution of these tissues to NST. Both isoproterenol-induced O2 consumption and cardiac output were lower in the dystrophic hamsters (13.0 +/- 0.4 vs. 18.2 +/- 0.68 ml O2 X g-0.67 X h-1 and 2.10 +/- 0.10 vs 2.98 +/- 0.16 ml X g-0.67 X min-1, respectively). Tissue blood flow was measured to brown fat, heart, skeletal muscle, liver, kidneys, adrenals, skin, and white fat. Isoproterenol was found to increase blood flows to brown fat, skeletal muscle, and cardiac muscle in normal animals and to brown fat and skeletal muscle in dystrophic hamsters, suggesting that these tissues contribute to NST. However, when corrected for body weight differences, blood flows during isoproterenol infusion to skeletal muscle and to cardiac muscle did not significantly differ between normal and dystrophic animals (2.71 +/- 0.29 vs. 3.33 +/- 0.42 and 2.81 +/- 0.25 vs. 1.85 +/- 0.24 ml X 100 g body wt-1, respectively). In contrast, normal brown adipose tissue had significantly elevated blood flows (3.50 +/- 0.39 vs. 2.28 +/- 0.27 ml X 100 g body wt-1). Thus these observations provide in vivo support for the conclusion that the reduced NST capacity of dystrophic hamsters is due, in large part, to a reduced thermogenic contribution of brown fat.
|Original language||English (US)|
|Journal||The American journal of physiology|
|Issue number||1 Pt 2|
|State||Published - Jul 1984|
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