Slide is from Jeffrey Sicat's lecture at OMA
Leptin and Insulin share same central feeding inhibitory and thermogenic pathway. Both are catabolic centrally. Insulin is weaker.
In Obese, Insulin triggers STEROIDOGENIC FACTOR (SF-1) expressing neurons of the VMH, resulting in inhibition of POMC neurons which promotes food intake and perpetuates obesity.
Vogt MC, Bruning JC CNS Insulin signaling
Trends Endo Metab 2013; 24(2) p 76-84
Clin Chim Acta. 2013 Feb 18;417:80-4. doi: 10.1016/j.cca.2012.12.007. Epub 2012 Dec 22.
Role of leptin and adiponectin in insulin resistance.
AbstractAdipose tissue is a major source of energy for the human body.
It is also a source of major adipocytokines adiponectin and leptin.
Insulin resistance is a condition in which insulin action is impaired in adipose tissue and is more strongly linked to intra-abdominal fat than to fat in other depots.
The expression of adiponectin decreases with increase in the adiposity.
Adiponectin mediates insulin-sensitizing effect through binding to its receptors AdipoR1 and AdipoR2, leading to activation of adenosine monophosphate dependent kinase (AMPK), PPAR-α, and presumably other yet-unknown signalling pathways.
Weight loss significantly elevates plasma adiponectin levels.
Reduction of adiponectin has been associated with insulin resistance, dyslipidemia, and atherosclerosis in humans.
The other major adipokine is leptin.
Leptin levels increase in obesity and subcutaneous fat has been a major determinant of circulating leptin levels.
The leptin signal is transmitted by the Janus kinase, signal transducer and activator of transcription ((JAK-STAT) pathway.
The net action of leptin is to inhibit appetite, stimulate thermogenesis, enhance fatty acid oxidation, decrease glucose, and reduce body weight and fat.