TY - JOUR
T1 - Insulin and metabolic efficiency in rats. I. Effects of sucrose feeding and BAT axotomy
AU - Bartness, T. J.
AU - Billington, C. J.
AU - Levine, A. S.
AU - Morley, J. E.
AU - Brown, D. M.
AU - Rowland, N. E.
PY - 1986
Y1 - 1986
N2 - The role of insulin and brown adipose tissue (BAT) thermogenesis in metabolic efficiency (ME, the efficiency of body wt gain) was examined in rats with varied basal insulin status. Long-lasting insulin was administered using a protocol that did not alter food intake, yet increased ME in both groups. Half the rats were fed sucrose to stimulate BAT growth and thermogenesis. Insulin overrode the exaggerated decrease in ME in sucrose-fed diabetics, with only partial attenuation in controls. Interscapular BAT (IBAT) lipoprotein lipase activity was decreased in diabetic rats, restored by insulin treatment, and not affected in controls. Sucrose-fed diabetics and controls had their IBAT sham or bilaterally surgically denervated. Insulin decreased the thermogenic potential of BAT [cytochrome oxidase activity (COA)] in intact controls and diabetics; in the latter, insulin restored COA independent of BAT innvervation. We conclude that 1) insulin can increase ME without an associated increase in energy intake, regardless of basal insulin status, 2) both insulin deficiency and excess decrease BAT thermogenic potential (COA), and 3) hyperinsulinemia-induced increases in ME may result from decreased BAT mitochondrial proliferation.
AB - The role of insulin and brown adipose tissue (BAT) thermogenesis in metabolic efficiency (ME, the efficiency of body wt gain) was examined in rats with varied basal insulin status. Long-lasting insulin was administered using a protocol that did not alter food intake, yet increased ME in both groups. Half the rats were fed sucrose to stimulate BAT growth and thermogenesis. Insulin overrode the exaggerated decrease in ME in sucrose-fed diabetics, with only partial attenuation in controls. Interscapular BAT (IBAT) lipoprotein lipase activity was decreased in diabetic rats, restored by insulin treatment, and not affected in controls. Sucrose-fed diabetics and controls had their IBAT sham or bilaterally surgically denervated. Insulin decreased the thermogenic potential of BAT [cytochrome oxidase activity (COA)] in intact controls and diabetics; in the latter, insulin restored COA independent of BAT innvervation. We conclude that 1) insulin can increase ME without an associated increase in energy intake, regardless of basal insulin status, 2) both insulin deficiency and excess decrease BAT thermogenic potential (COA), and 3) hyperinsulinemia-induced increases in ME may result from decreased BAT mitochondrial proliferation.
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U2 - 10.1152/ajpregu.1986.251.6.r1109
DO - 10.1152/ajpregu.1986.251.6.r1109
M3 - Article
C2 - 3024508
AN - SCOPUS:85088667948
SN - 0363-6119
VL - 251
SP - R1109-R1117
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 6 (20/6)
ER -