Abstract
Adiposity increases in middle age and declines in extreme age in both men and women. Visceral fat deposits increase throughout the lifespan in both males and females. Aging is associated with a decline in the expression of genes that produce preadipocyte differentiation and in lipid accumulation, resulting in a decreased fat cell size. The decline in lipogenesis is due both to a decrease in triglyceride uptake into fat cells secondary to a decline in lipoprotein lipase activity, decreased glucose transport, and fatty acid synthesis. There is a decrease in lipid oxidation with aging. Leptin levels rise in middle age and decline in old age in females, while in males leptin levels continue to increase probably due to the decline in testosterone. Resting metabolic rate declines with aging. This decline is greater in men than women. The role of brown fat and UCP1 (uncoupling protein 1) is unknown in adult humans, but in rodents beta-3 adrenergic responsiveness of brown fat decreases with aging while the response to cold induced thermogenesis is maintained. Whether alterations in UCP2 and UCP3 occur with aging remain to be determined.
Original language | English |
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Pages (from-to) | 695-704 |
Number of pages | 10 |
Journal | Facts, Research and Intervention in Geriatrics |
Volume | 2000 |
Issue number | PART 2 |
Publication status | Published or Issued - 2000 |
ASJC Scopus subject areas
- Geriatrics and Gerontology