Leptins and Obesity

Our Leptin and Leptin Receptor Markers have proven effective for researchers studying root causes of obesity. In this reference the authors show an interesting twist regarding the impact of endothial vs neuronal leptin signaling: Weihong Pan, Hung Hsuchou, Germaine G. Cornelissen-Guillaume, Bhavvani Jayaram, Yuping Wang, Hong Tu, Franz Halberg, Xiaojun Wu, Streamson C. Chua Jr., and Abba J. Kastin. Endothelial leptin receptor mutation provides partial resistance to diet-induced obesity. Published online before print February 2012, doi: 10.​1152/​japplphysiol.​00590.​2011.
...chicken anti-ObRb (1:100, Neuromics)...

Highlights: Leptin, a polypeptide hormone produced mainly by adipocytes, has diverse effects in both the brain and peripheral organs, including suppression of feeding. Other than mediating leptin transport across the blood-brain barrier, the role of the endothelial leptin receptor remains unclear. We recently generated a mutant mouse strain lacking endothelial leptin receptor signaling, and showed that there is an increased uptake of leptin by brain parenchyma after its delivery by in-situ brain perfusion. Here, we tested the hypothesis that endothelial leptin receptor mutation confers partial resistance to diet-induced obesity. These ELKO mice had similar body weight and percent fat as their wildtype littermates when fed with rodent chow, but blood concentrations of leptin were significantly elevated. In response to a high fat diet, wildtype mice had a greater gain of body weight and fat than ELKO mice . As shown by metabolic chamber measurement, the ELKO mice had higher oxygen consumption, carbon dioxide production, and heat dissipation, although food intake was similar to that of the wildtype mice and locomotor activity was even reduced. This indicates that the partial resistance to diet-induced obesity was mediated by higher metabolic activity in the ELKO mice. Since neuronal leptin receptor knockout mice show obesity and diabetes, the results suggest that endothelial leptin signaling shows opposite effects from that of neuronal leptin signaling, with a facilitatory role in diet-induced obesity.


Obesity is a growing health problem and will continue to drive up costs. Research like this could help find effective and log term solutions for helping with weight loss.

Aging-Caloric Restriction and BDNF-Leptin

As we age, selective BDNF receptors increase in the the dorsal vagal complex (DVC), the brainstem center mediating the satiety reflex. Aging also affects the suppressor of cytokine signaling-3. This results in abnormal responses to BDNF and Leptin Signaling.

In this study, the investigators found that by restricting calories in rats, DVC BDNF immunoreactive concentrations were elevated and resulting in satiety threshold stability.  This indicates functional desensitization of the DVC to these signals: Karine Bédard, Stéphanie Segura, Stéphanie Mahaut, Catherine Tardivel, Guylaine Ferland, Bruno Lebrun, Pierrette Gaudreau. Effects of aging and caloric restriction on brainstem satiety center signals in rats. Mechanisms of Ageing and Development. dx.doi.org/10.1016/j.mad.2012.01.004.

The authors used our BDNF Antibody to determine expression in the DVC.....goat serum and 0.3% Triton-X-100) (Sigma–Aldrich), overnight at 4 °C with chicken anti-rat BDNF antibody (Neuromics, Edina, MN; diluted 1/200 in blocking buffer), rinsed 3× 10 min in fresh PBS and incubated for 2 h, in the dark...

These findings could lead to potential therapies based on modulating BDNF expression in the DVC.