Lipolysis sensation by white fat afferent nerves triggers brown fat thermogenesis.

OBJECTIVE: Metabolic challenges, such as a cold environment, stimulate sympathetic neural efferent activity to white adipose tissue (WAT) to drive lipolysis, thereby increasing the availability of free fatty acids as one source of fuel for brown adipose tissue (BAT) thermogenesis. WAT is also innervated by sensory nerve fibers that network to metabolic brain areas; moreover, activation of these afferents is reported to increase sympathetic nervous system outflow. However, the endogenous stimuli sufficient to drive WAT afferents during metabolic challenges as well as their functional relation to BAT thermogenesis remain unknown. METHOD: We tested if local WAT lipolysis directly activates WAT afferent nerves, and then assessed whether this WAT sensory signal affected BAT thermogenesis in Siberian hamsters (Phodopus sungorus). RESULTS: 2-deoxyglucose, a sympathetic nervous system stimulant, caused ß-adrenergic receptor dependent increases in inguinal WAT (IWAT) afferent neurophysiological activity. In addition, direct IWAT injections of the ß3-AR agonist CL316,243 dose-dependently increased: 1) phosphorylation of IWAT hormone sensitive lipase, an indicator of SNS-stimulated lipolysis, 2) expression of the neuronal activation marker c-Fos in dorsal root ganglion neurons receiving sensory input from IWAT, and 3) IWAT afferent neurophysiological activity, an increase blocked by antilipolytic agent 3,5-dimethylpyrazole. Finally, we demonstrated that IWAT afferent activation by lipolysis triggers interscapular BAT thermogenesis through a neural link between these two tissues. CONCLUSIONS: These data suggest IWAT lipolysis activates local IWAT afferents triggering a neural circuit from WAT to BAT that acutely induces BAT thermogenesis.

The rise of novelty in ecosystems.

Rapid and ongoing change creates novelty in ecosystems everywhere, both when comparing contemporary systems to their historical baselines, and predicted future systems to the present. However, the level of novelty varies greatly among places. Here we propose a formal and quantifiable definition of abiotic and biotic novelty in ecosystems, map abiotic novelty globally, and discuss the implications of novelty for the science of ecology and for biodiversity conservation. We define novelty as the degree of dissimilarity of a system, measured in one or more dimensions relative to a reference baseline, usually defined as either the present or a time window in the past. In this conceptualization, novelty varies in degree, it is multidimensional, can be measured, and requires a temporal and spatial reference. This definition moves beyond prior categorical definitions of novel ecosystems, and does not include human agency, self-perpetuation, or irreversibility as criteria. Our global assessment of novelty was based on abiotic factors (temperature, precipitation, and nitrogen deposition) plus human population, and shows that there are already large areas with high novelty today relative to the early 20th century, and that there will even be more such areas by 2050. Interestingly, the places that are most novel are often not the places where absolute changes are largest; highlighting that novelty is inherently different from change. For the ecological sciences, highly novel ecosystems present new opportunities to test ecological theories, but also challenge the predictive ability of ecological models and their validation. For biodiversity conservation, increasing novelty presents some opportunities, but largely challenges. Conservation action is necessary along the entire continuum of novelty, by redoubling efforts to protect areas where novelty is low, identifying conservation opportunities where novelty is high, developing flexible yet strong regulations and policies, and establishing long-term experiments to test management approaches. Meeting the challenge of novelty will require advances in the science of ecology, and new and creative. conservation approaches.

Female puberty acceleration by male odour in mice: neural pathway and behavioural consequences.

In female mice, exposure to male chemosignals results in early puberty onset characterized by advanced vaginal opening and higher uterine weight. Evidence suggests that the male chemosignals responsible for acceleration of female puberty are androgen-dependent, but not all of the compounds that contribute to puberty acceleration have been identified. The male chemosignals are primarily detected and processed by the vomeronasal system including the vomeronasal organ, the accessory olfactory bulb and the medial amygdala. By contrast, the mechanism by which this olfactory information is integrated in the hypothalamus is poorly understood. In this context, the recent identification of the neuropeptide kisspeptin as a gatekeeper of puberty onset may provide a good candidate neuropeptide system for the transmission of chemosensory information to the gonadotrope axis.

Kisspeptin: a new neuronal target of primer pheromones in the control of reproductive function in mammals.

Pheromones are known to trigger either short-term behavioral responses, usually referred to as "releaser effects", or more long-term physiological changes, known as "primer effects", which especially affect reproductive function at the level of the gonadotrope axis. The precise mechanisms through which pheromones interact with the gonadotrope axis in the hypothalamus is not fully known. We propose that the neuropeptide Kisspeptin, could be a specific target of primer pheromones, allowing these pheromones to modulate the gonadotrope axis and GnRH activity. This emerging hypothesis is discussed in the context of puberty acceleration in female mice and the male effect in female ungulates (sheep or goat). These examples have been chosen to illustrate the diversity of the reproductive contexts in mammals and potential mechanisms affected by primer effects at the level of the gonadotrope axis.

Signals that link energy to reproduction: gastric fill, bulk intake, or caloric intake?

Reproductive processes are inhibited by deficits in the availability of metabolic fuels, and this inhibition increases the chances of survival during energetic challenges and optimizes reproductive success by delaying energetically costly processes until fuels become available. The mechanisms that link energy availability to reproduction are unknown, and thus, in this study we tested the hypothesis that estrous cycles are most sensitive to sensory signals from bulk intake and gastric fill as opposed to signals from caloric intake or the availability of intracellular oxidizable fuels. The caloric content of a standard laboratory chow diet was diluted by 25, 50, or 75% with the largely indigestible fiber, cellulose, and fed to food-deprived, female hamsters throughout day 2 of the estrous cycle (ovulation and estrous behavior normally occur on day 4). The bulk intake/gastric fill hypothesis was not supported because bulk intake increased the more the diet was diluted, whereas the frequency of hamsters showing normal 4-day estrous cycles decreased with diet dilution, along with decreases in caloric intake and in plasma insulin concentrations. Rate of gastric emptying did not change significantly with diet dilution. Although consumption of a diluted diet significantly lengthened the estrous cycle, it did not affect incidence of pregnancy, litter size or pup weight. Thus, when hamsters ingest sufficient energy to support estrous behavior, they fully recover reproductive potential. In summary, neither bulk intake nor gastric fill provides critical signals necessary for reproduction, consistent with the idea that reproduction is primarily responsive fuel availability.