Hypothalamic neuropeptide systems and anticipatory weight change in Siberian hamsters

Seasonal animals are able both to programme changes in body weight in response to annual changes in photoperiod (anticipatory regulation) and to correct changes in body weight caused by imposed energetic demand (compensatory regulation). Experimental evidence from the Siberian hamster suggests that seasonally appropriate body weight is continually reset according to photoperiodic history, even when actual body weight is driven away from this target weight by manipulation of energy intake. These characteristics constitute the "sliding set point" of seasonal body weight regulation. To define the mechanisms and molecules underlying anticipatory body weight regulation, we are investigating the involvement of hypothalamic systems with an established role in the compensatory defence of body weight. Weight loss or restricted growth induced by short days (SD) results in low circulating leptin compared with long day (LD) controls. However, this chronic low leptin signal is read differently from acute low leptin resulting from food deprivation; leptin receptor gene expression in the hypothalamic arcuate nucleus (ARC) is lower in SD, whereas food deprivation increases expression levels, suggesting changes in sensitivity to leptin feedback. SD alterations in mRNA levels for a number of hypothalamic neuropeptide and receptor genes appear counter-intuitive for a SD body weight trajectory. However, early increases in ARC cocaine-and amphetamine-regulated transcript (CART) gene expression in SDs could be involved in driving body weight loss or growth restriction. The sites of photoperiod interaction with energy balance neuronal circuitry and the neurochemical encoding of body weight set point require full characterisation. Study of anticipatory regulation in seasonal animals offers new insight into body weight regulation across mammalian species, including man.