Diabesity
In general the work of the group has been focused in different lines of work aiming to delineate new mechanisms regulating energy balance.
We focus in uncovering the mechanisms by which the CNS regulate peripheral metabolism (e.g. Liver, Wat, BAT) and how afferent peripheral signals (e.g. gonadal hormones, gastrointestinal hormones, insulin etc.) influence food intake and food behavior at central level.
Actually we are more focus in new components of this system like cell cycle regulators or new antagonist of ghrelin system and the influence in the development of metabolic diseases: type2 diabetes and NAFLD (non alcoholic fatty liver disease).
Research Lines
We described that the deficiency of p107 (a cell cycle regulator member of pocket proteins like Rb and p130) triggered brown fat thermogenesis activation and improved hepatic metabolism in high caloric conditions. Now, we are investigating its specific metabolic role in the liver and adipocytes highlighting two aspects:
a) the relevance of p107 in the crosstalk between adipose tissue and liver.
b) delineating the effects of p107 from organ to cell-specificity.
The new discovery of the ghrelin antagonist LEAP-2 allowed us to explore:
a) The regulatory role of LEAP-2 in energy homeostasis and its metabolic actions in peripheral metabolism in organs like liver and WAT.
b) In human, to assess LEAP2 levels as a new circulating biomarker in normal and in patients with different diseases states linked to alterations in energy homeostasis.
Members
Selected publications
LEAP-2 Counteracts Ghrelin-Induced Food Intake in a Nutrient, Growth Hormone and Age Independent Manner
p107 Deficiency Increases Energy Expenditure by Inducing Brown-Fat Thermogenesis and Browning of White Adipose Tissue
Prolonged breastfeeding protects from obesity by hypothalamic action of hepatic FGF21
Obesity induces resistance to central action of BMP8B through a mechanism involving the BBSome.
O-GlcNAcylated p53 in the liver modulates hepatic glucose production