Open AccessRats that are predisposed to excessive obesity show reduced (leptin‐induced) thermoregulation even in the preobese state
Author(s) -
Git Kathy C.G.,
Outer Johannes A.,
WolterinkDonselaar Inge G.,
Luijendijk Mieneke C. M.,
Schéle Erik,
Dickson Suzanne L.,
Adan Roger A. H.
Publication year - 2019
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.14102
Subject(s) - leptin , thermogenesis , endocrinology , medicine , thermoregulation , hypothalamus , brown adipose tissue , obesity , adipose tissue , adipokine , biology
Both feeding behavior and thermogenesis are regulated by leptin. The sensitivity to leptin's anorexigenic effects on chow diet was previously shown to predict the development of diet‐induced obesity. In this study, we determined whether the sensitivity to leptin's anorexigenic effects correlates with leptin's thermogenic response, and if this response is exerted at the level of the dorsomedial hypothalamus ( DMH ), a brain area that plays an important role in thermoregulation. Based on the feeding response to injected leptin on a chow diet, rats were divided into leptin‐sensitive ( LS ) and leptin‐resistant ( LR ) groups. The effects of leptin on core body, brown adipose tissue ( BAT ) and tail temperature were compared after intravenous versus intra‐ DMH leptin administration. After intravenous leptin injection, LS rats increased their BAT thermogenesis and reduced heat loss via the tail, resulting in a modest increase in core body temperature. The induction of these thermoregulatory mechanisms with intra‐ DMH leptin was smaller, but in the same direction as with intravenous leptin administration. In contrast, LR rats did not show any thermogenic response to either intravenous or intra‐ DMH leptin. These differences in the thermogenic response to leptin were associated with a 1°C lower BAT temperature and reduced UCP 1 expression in LR rats under ad libitum feeding. The preexisting sensitivity to the anorexigenic effects of leptin, a predictor for obesity, correlates with the sensitivity to the thermoregulatory effects of leptin, which appears to be exerted, at least in part, at the level of the DMH .