Abhiram Sahu, Ph.D.. |
The major research emphasis of this laboratory is directed towards understanding the mechanisms of leptin and insulin signaling in the hypothalamus with reference to feeding, obesity, diabetes and reproduction. Recently, Dr. Sahu identified several hypothalamic peptidergic systems as potential targets of leptin signaling. This laboratory has also identified PI3K-phosphodiesterase 3B-cAMP pathway, as a novel mechanism of leptin signaling in the hypothalamus Since leptin resistance may be the major cause of obesity and related disorders in human, this laboratory is currently using a rat model to address whether this is due to an alteration in leptin receptor activity and/ or defects in leptin signal transduction mechanisms (e.g. JAK/STAT pathway and PI3K-PDE3B-cAMP pathway) in specific neuronal systems. Another area of research is to elucidate the neuroendocrine mechanisms that are involved in female reproductive aging. Since neuropeptide Y (NPY), is one of the key excitatory signals that control secretion of GnRH and LH, major emphasis has been given on this neuropeptide to test the hypothesis that alterations in secretion and action of this peptide underlie the cause of reproductive senescence.
- Sahu, A. (2006). Alteration in hypothalamic neuropeptide Y (NPY) secretion may underlie the female reproductive aging: induction of steroid-induced luteinizing hormone surge by NPY in ovariectomized old rats. J. Neuroendocrinol. 18:584-593.
- Sahu, A. and Metlakunta, A. R. (2005). Hypothalamic Phosphatidylinositol 3-kinase-Phosphodiesterase 3B-cyclic AMP pathway of leptin signaling in the hypothalamus is impaired following chronic central leptin infusion. J. Neuroendocrinol. 17:720-726
- Sahu, A, Nguyen, L. and O'Doherty, R.M. (2002). Nutritional regulation of hypothalamic leptin receptor gene expression is defective in diet-induced obesity. J. Neuroendocrinol. 14:887-893.
- Sahu, A. (2002). Interactions of neuropeptide Y, orexin A (hypocretin-1) and melanin-concentrating hormone on feeding in rats. Brain Research, 944:232-238.
- Sahu, A. (2002). Resistance to the satiety action of leptin following chronic central leptin infusion is associated with the development of leptin resistance in neuropeptide Y neurones. J. Neuroendocrinol. 14:796-804.
- Zhao, A.Z., Huan, J-N., Gupta, S., Pal, R. and Sahu, A. (2002). A Phosphatidylinositol 3-K - phosphodiesterase 3B - cyclic AMP pathway is involved in hypothalamic action of leptin on feeding. Nature Neuroscience, 5:727-728.
- Sahu, A., Carraway, R.E. and Wang, Y-P. (2001). Evidence that neurotensin mediates the central effect of leptin on food intake in rat. Brain Research, 888:343-347.
- Sahu, A. (2000). Evidence suggesting that the potentiating action of neuropeptide Y on luteinizing hormone (LH)-releasing hormone-induced LH release remains unaltered in aged female rats. J. Neuroendocrinol. 12:495-500.
- Sahu, A. (1998). Absence of increased hypothalamic nitric oxide synthase gene expression during the preovulatory LH surge in middle-aged rats. NeuroReport, 9:4019-4023.
- Sahu, A. (1998). Evidence suggesting that galanin (GAL), melanin-concentrating hormone (MCH), proopiomelanocortin (POMC), neurotensin (NT) and neuropeptide Y (NPY) are targets of leptin signaling in the hypothalamus. Endocrinology, 139:795-798.
- Sahu, A. (1998). Leptin decreases food intake induced by melanin-concentrating hormone (MCH), galanin (GAL) and neuropeptide Y (NPY) in the rat. Endocrinology, 139:4739-4742.
- Sahu, A. and Kalra, S.P. (1998). Absence of increased neuropeptide Y neuronal activity before and during the luteinizing hormone (LH) surge may underlie the attenuated preovulatory LH surge in middle-aged rats. Endocrinology, 139:696-702.


