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Department of Medicine, Divisions of 1 Geriatrics, 2 Endocrinology, and the Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, New York 10461
Increase in fat mass (FM) and changes in
body composition may account for the age-associated impairment in
insulin action on muscle glycogen storage. We wish to examine whether
preventing the increase in FM abolishes this defect seen with aging. We
studied the novel aging model of F1 hybrids of BN/F344 NIA rats fed ad libitum (AL) at 2 (weighing 259 ± 17 g), 8 (459 ± 17 g), and 20 (492 ± 10 g) mo old. To prevent the age-dependent growth in FM, rats were caloric restricted (CR) at 2 mo by decreasing their daily
caloric intake by 45% (weighing 292 ± 5 g at 8 mo, 294 ± g at
20 mo). As designed, the lean body mass (LBM) and %FM remained unchanged through aging (8 and 20 mo old) in the CR rats and was similar to that of 2-mo-old AL rats. However, 8- and 20-mo-old AL-fed
rats had three- to fourfold higher FM than both CR groups. Peripheral
insulin action at physiological hyperinsulinemia was determined (by 3 mU · kg
1 · min1
insulin clamp). Prevention of fat accretion maintained glucose uptake
(Rd; 29 ± 2, 29 ± 2, and 31 ± 4 mg · kg
LBM1 · min1)
and glycogen synthesis rates (GS, 12 ± 1, 12 ± 1, and 14 ± 2 mg · kg
LBM1 · min1)
at youthful levels (2 mo AL) in 8- and 20-mo-old CR rats, respectively. These levels were significantly increased
(P < 0.001) compared with AL rats
with higher %FM (Rd, 22 ± 1 and 22 ± 2 and GS, 7 ± 1 and 8 ± 2 mg · kg
LBM1 · min1
in 8- and 20-mo-old rats, respectively). The increase in whole body GS
in age-matched CR rats was accompanied by ~40% increased accumulation of
[3H]glucose into
glycogen and a similar increase in insulin-induced muscle glycogen
content. Furthermore, the activation of glycogen synthase increased,
i.e., ~50% decrease in the Michaelis constant, in both CR groups
(P < 0.01). We conclude that chronic
CR designed to prevent an increase in storage of energy in fat
maintained peripheral insulin action at youthful levels, and aging per
se does not result in a defect on the pathway of glycogen storage in
skeletal muscle.
fat mass; caloric restriction; lean body mass; insulin-mediated glycogen synthesis
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