Page 87 - CIBEROBN2016-ENG

Most relevant scientific articles
• Gulfo J., Ledda A., Serra E., Cabot C., Esteve M., Grasa M. Altered lipid partitioning and glucocorticoid availability in CBG-deficient male mice with diet-induced obesity. Obesity. 2016;.
• Calderón-Domínguez M., Sebastián D., Fucho R., Weber M., Mir J.F., García-Casarrubios E. et al. Carnitine palmitoyltransferase 1 increases lipolysis, UCP1 protein expression and mitochondrial activity in brown adipocytes. PLoS ONE. 2016;11(7).
• Arriaran S., Agnelli S., Remesar X., Alemany M., Fernández-López J.A. White adipose tissue urea cycle activity is not affected by one-month treatment with a hyperlipidic diet in female rats. Food and Function. 2016;7(3):1554-1563.
• Casals N., Zammit V., Herrero L., Fado R., Rodríguez-Rodríguez R., Serra D. Carnitine palmitoyltransferase 1C: From cognition to cancer. Progress in Lipid Research. 2016;61:134-148.
• Sabater D., Agnelli S., Arriaran S., Romero M.M., Fernández-López J.A., Alemany M. et al. Cafeteria diet induce changes in blood flow that are more related with heat dissipation than energy accretion. PeerJ. 2016;2016(3).
Hightlights
Role of CPTI in the development of obesity-induced insulin resistance and type 2 diabetes. We study that enhancing fatty acid oxidation in liver, in brown adipose tissue can be new therapies against obesity.
In the study of the effect of overexpression of CPT1 in animal models prone to obesity prevention and treatment of obesity, it has been observed that in mice in which obesity is induced by fat diet and which has the CPT1A overexpressed exhibit a reversal of hyperinsulinemia, hyperglycemia and an almost complete reversal of hepatic steatosis accompanied by a slight decrease in weight of the animals.
We also study the role of CPT1A and CPT1C in the hypothalamus in the control of food intake and energy expenditure.
We study of C75 derivatives as potential drugs against obesity by their interaction with CPT1 at the hypothalamus.
CBG deficiency promotes the redistribution of lipids from the subcutaneous tissue to the visceral tissue in a context in which excess lipids modulate the expression of the 11-beta hydroxy steroid dehydrogenase and hence the activity of the glucocorticoids.
We have described the presence of all the enzymes of the urea cycle in adipose tissue, although there are differences depending on their body location and their response to energy availability. In any case, adipose tissue, although dispersed organ, seems to be subject to uniform control.
The incubation of cells isolated from adipose tissue, in periods of up to 48 hours, has allowed us to determine its high capacity to produce lactate and glycerol. But we have also been able to determine that the active cell volume of the adipocytes (non-fatty) represents only 1.3% of the tissue.
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