Dim light at night exaggerates weight gain and inflammation associated with a high-fat diet in male mice.

Elevated nighttime light exposure is associated with symptoms of metabolic syndrome. In industrialized societies, high-fat diet (HFD) and exposure to light at night (LAN) often cooccur and may contribute to the increasing obesity epidemic. Thus, we hypothesized that dim LAN (dLAN) would provoke additional and sustained body mass gain in mice on a HFD. Male mice were housed in either a standard light/dark cycle or dLAN and fed either chow or HFD. Exposure to dLAN and HFD increase weight gain, reduce glucose tolerance, and alter insulin secretion as compared with light/dark cycle and chow, respectively. The effects of dLAN and HFD appear additive, because mice exposed to dLAN that were fed HFD display the greatest increases in body mass. Exposure to both dLAN and HFD also change the timing of food intake and increase TNFα and MAC1 gene expression in white adipose tissue after 4 experimental weeks. Changes in MAC1 gene expression occur more rapidly due to HFD as compared with dLAN; after 5 days of experimental conditions, mice fed HFD already increase MAC1 gene expression in white adipose tissue. HFD also elevates microglia activation in the arcuate nucleus of the hypothalamus and hypothalamic TNFα, IL-6, and Ikbkb gene expression. Microglia activation is increased by dLAN, but only among chow-fed mice and dLAN does not affect inflammatory gene expression. These results suggest that dLAN exaggerates weight gain and peripheral inflammation associated with HFD.

Short day-length increases sucrose consumption and adiposity in rats fed a high-fat diet.

BACKGROUND: Photoperiod, i.e., the relative day-length per 24h, may modulate the metabolic responses to high-fat diet (HFD) and sucrose consumption. METHODS: To test this hypothesis, hormonal changes, fat accretion and sucrose intake were measured in rats exposed to short- or long-day for 4 weeks and fed with a standard high-carbohydrate low-fat pelleted diet (high-carbohydrate diet (HCD)) or a high-fat, medium-carbohydrate pelleted diet (HFD), with or without free access to 10% sucrose solution in addition to water available ad libitum. RESULTS: Plasma leptin and adiposity index, defined as epididymal white fat expressed as percentage of body mass, were markedly increased only in HFD-fed animals drinking sucrose under short, but not long, photoperiods. Voluntary ingestion of sucrose under short days was greater in HFD rats compared with HCD animals over the experiment, while a trend for the opposite effect was visible under long days. Total energy intake was not changed overall, as rats proportionally decreased chow intake when they drank sucrose. A noteworthy exception was the HFD group with sucrose access under short days that significantly increased their total calorie intake. Fasting blood glucose was generally unaltered, except for an increase in HFD-fed animals drinking sucrose under long days compared to control animals, suggesting a decrease in glucose tolerance. Insulin resistance was not yet affected by nutritional or photoperiodic conditions after 4 experimental weeks. CONCLUSIONS: Even if photoperiod cannot be considered as an obesogenic environmental factor per se, the metabolic effects resulting from the combination of high-fat feeding and voluntary intake of sucrose were dependent on day-length. Exposure to short days triggers a larger increase of sucrose ingestion and hyperleptinemia in rats fed with HFD compared to the control diet. Considering that the cardinal symptoms of winter depression include carbohydrate craving and increased adiposity, the present data provide an experimental basis for developing new animal models of seasonal affective disorder.

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.