The effect of ageing on the orcadian control of food intake in the rat

Rietveld, W.J.; Ruis, J.F.; Buijs, P.

doi:10.1080/09291018809359986

Cited by 7 publications

(3 citation statements)

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“…Age-dependent changes in the free-running period of locomotor activity in several mammals have been reported, although the effects vary among species. However, in rats, aging consistently shortens the free-running period (21)(22)(23)(24).…”

Section: Discussionmentioning

confidence: 99%

“…In several species of mammals, aging affects the amplitude and phase of circadian rhythms (18)(19)(20). The period of the circadian locomotor activity rhythm is shortened in aged rats (21)(22)(23)(24) and in aged hamsters by most reports (20,(25)(26)(27)(28); however, two studies of hamsters failed to reveal age-related changes in period (29,30). The effect of aging on the free-running period in mice has not been consistent (18,20).…”

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confidence: 96%

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Effects of aging on central and peripheral mammalian clocks

Yamazaki

Straume

Tei

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

279

220

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Circadian organization changes with age, but we do not know the extent to which age-related changes are the result of alterations in the central pacemakers, the peripheral oscillators, or the coupling mechanisms that hold the system together. By using transgenic rats with a luciferase (luc) reporter, we assessed the effects of aging on the rhythm of expression of the Period 1 (Per1) gene in the suprachiasmatic nucleus (SCN) and in peripheral tissues. Young (2 months) and aged (24 -26 months) Per1-luc transgenic rats, entrained to light-dark cycles, were killed, and tissues were removed and cultured. Per1-luc expression was measured from 10 tissues. In the SCN, the central mammalian pacemaker, Per1-luc expression was robustly rhythmic for more than 7 weeks in culture. The only difference between SCN rhythmicity in young and old rats was a small but significant age-related shortening of the free-running period. Circadian rhythmicity in some peripheral tissues was unaffected by aging, whereas rhythmicity in other tissues was either phase advanced relative to the light cycle or absent. Those tissues that were arrhythmic could be induced to oscillate by application of forskolin, suggesting that they retained the capacity to oscillate but were not being appropriately driven in vivo. Overall, the results provide new insights into the effects of aging on the mammalian circadian system. Aging seems to affect rhythms in some but not in all tissues and may act primarily on interactions among circadian oscillators, perhaps attenuating the ability of the SCN to drive damped oscillators in the periphery.T he SCN is a circadian pacemaker structure that drives myriad behavioral and physiological rhythms in mammals (1). Surgical destruction of the SCN abolishes most circadian rhythms (2-5); however, some rhythms persist including mitosis in cornea and gut and disk shedding in the retina (6, 7). Circadian rhythms in wheel-running behavior, absent following complete SCN lesions, reappear when methamphetamine is provided chronically to SCN-lesioned rats (8). Furthermore, SCN-lesioned rats express a rhythm in food-anticipatory activity when exposed to restricted feeding and later fasted (9). Collectively, these observations reveal the existence of extra-SCN circadian oscillators. More recent results suggest that they may be present in most mammalian cells and tissues (10,11).Rapid progress in the cloning and identification of clock genes has revealed that these genes are expressed not only in the SCN but in many peripheral tissues as well (12). The recent development of a transgenic rat model allows for the continuous monitoring of Per1 transcription through use of a luciferase reporter (13). By using this methodology, it was discovered that several peripheral structures, as well as extra-SCN brain areas, exhibit circadian oscillations in vitro (13-15). Consequently, there is now direct evidence that the mammalian circadian system is composed of multiple circadian oscillators, a central pacemaker in the SCN, and damped oscillators i...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 96%

Effects of aging on central and peripheral mammalian clocks

Yamazaki

Straume

Tei

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

279

220

View full text Add to dashboard Cite

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“…27,28 A fragmentation of the circadian pattern of feeding is encountered both in genetic obesity 11 and in aging. 29 Both obese 30 and aged 31 rats are less responsive to administration of exogenous substances acting on feeding such as NPY.…”

Section: Introductionmentioning

confidence: 99%

Combined effect of obesity and aging on feeding-induced monoamine release in the rostromedial hypothalamus of the Zucker rat

et al. 1998

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OBJECTIVE: The obesity of the Zucker rat is associated with numerous metabolic and neurochemical disturbances involving the central transmitters regulating feeding behaviour. Among them, the release of satiety-related monoamines from the median hypothalamus in response to a meal is enhanced in obese, as compared to normal, rats as though larger amounts of these amines were necessary to bring about satiety in obese rats. Besides, the obese Zucker rat has often been described as shorter-living than its lean congener. One of the reasons for the shorter longevity of the obese rat was investigated in this study: it could be an aggravation of its obesity-related central disturbances with age. METHODS: We assessed the response to a meal of the hypothalamic monoamines, dopamine and serotonin, in young (four month old) and old (twelve month old) lean (Fa-Fa) and obese (fa-fa) Zucker rats. The in vivo technique of microdialysis was used to combine behavioural recordings and continuous neurochemical assays. RESULTS: The exacerbation of monoamine release observed in young obese rats in response to a meal was no longer found in old obese rats. Serotonin increase during a meal weakened with aging, especially in obese rats. Dopamine (DA) response to a meal was completely reversed in old obese rats, with a decrease instead of the increase observed in the three other groups. CONCLUSION: The decrease of monoaminergic response to a meal with age is apparently the opposite to the enhanced release related to obesity. However, this does not correspond to an amelioration of the hyperphagia of the obese rats with age, as we could observe in parallel behavioural experiments, but rather to a decrease in neurotransmitter metabolism and thus in neuronal functioning.

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