Leptin and seasonal mammals.

Seasonal mammals commonly exhibit robust annual cycles of adiposity, food intake and energy metabolism. These cycles are driven by changes in the external daylength signal, which generates a diurnal melatonin profile and acts on neuroendocrine pathways. The white adipose tissue hormone leptin reflects overall adiposity in seasonal mammals, and consequently undergoes significant seasonal fluctuations in secretion. The seasonally breeding Siberian (Djungarian) hamster is a convenient laboratory model to study the effect of a seasonal time-keeping clock on energy metabolism, appetite regulation and the control of adiposity. We have shown that administration of exogenous leptin at physiological doses induces significant loss of adipose tissue for short-day housed winter-like hamsters in which endogenous adipose tissue and leptin concentrations are already low. By contrast, long-day housed hamsters with high adipose tissue reserves are refractory to the effects of leptin. This phenomenon of seasonal leptin resistance appears to be a general feature of other seasonally breeding mammals, and may reflect the operation of an annual timer controlling leptin uptake and/or action on central nervous system signal transduction pathways. The mobilization of fat by leptin in short-day housed hamsters is not associated with changes in expression in either anorexic or anabolic peptides expressed in leptin-receptor rich structures in the arcuate region of the hypothalamus, and suggests that leptin may target other structures. These data contrast with studies, which show that homeostatic mechanisms in response to feed-restriction induce changes in hypothalamic peptides in a similar manner to nonphotoperiodic species. Thus, the long-term seasonal regulation of body weight set point and leptin feedback may operate through separate pathways to those responsible for acute responses to food restriction.