Quote (Balla @ Sep 26 2014 08:00am)
"Leptin and aging: Review and questions with particular emphasis on its role in the central regulation of energy balance"
http://a.pomf.se/gkttdu.pdfThought I'd bring a little attention to this paper again, forgot to do this before.
There's some pretty interesting tid-bits, especially regarding insulin-leptin crosstalk. I'll just quote some parts from the paper:
"Insulin resistance in immortalized hypothalamic neurons (induced by chronic insulin exposure) attenuates activity of the PI3K pathway by suppressing phosphorylation of AKT that is required for leptin mediated transcriptional regulation of neurons. In addition, chronic stimulation of insulin receptors lead to an increase in SOCS3 levels, which are known to inhibit both leptin and insulin signal transduction. And vice versa, chronic exposure to elevated leptin levels in the hypothalamus can negatively impact insulin signaling via reducing the interaction of the insulin receptor with IRS2 and increasing its association with SOCS3."
"Moreover, in a mouse model of total leptin receptor ablation, separate restoration of leptin receptors on POMC neurons of the arcuate nucleus resulted in normalization of peripheral insulin sensitivity, in an increase in metabolic rate (indicated by oxygen consumption) but failed to normalize food intake."
"The possibility of fructose-induced impairment of the AMPK pathway in leptin signaling, that of increased activation of the hexosamine biosynthetic pathway with potential increases in O-linked glycosylation of signaling proteins has been suggested by Vasselli et al. (2013). Levin et al. (2004) described leptin resistance due to a high-fat diet in the presence of maintained leptin transport through the BBB and before the onset of obesity in obesity prone rats."