Effects of fasting, leptin, and insulin on AGRP and POMC peptide release in the hypothalamus

Breen, Tracy L.; Conwell, Irene M.; Wardlaw, Sharon L.

doi:10.1016/j.brainres.2004.11.008

Cited by 70 publications

(46 citation statements)

References 32 publications

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“…Using Western blot analysis, we detected a robust induction of AKT phosphorylation (on Thr308 and Ser473) after insulin administration ( Figure 5A). An inhibitor of AKT (AKTi) reduced the production of POMC and BEP in day-38 neurons ( Figure 5B), indicating that neuropeptide production in these neurons might be regulated by metabolic signals (40)(41)(42).…”

Section: Nkx21 Gfp/w Hesc-derived Neurons Can Sense and Respond To Imentioning

confidence: 99%

Differentiation of hypothalamic-like neurons from human pluripotent stem cells

Wang¹,

Meece²,

Williams³

et al. 2015

J. Clin. Invest.

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125

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Section: Nkx21 Gfp/w Hesc-derived Neurons Can Sense and Respond To Imentioning

confidence: 99%

Differentiation of hypothalamic-like neurons from human pluripotent stem cells

Wang¹,

Meece²,

Williams³

et al. 2015

J. Clin. Invest.

Self Cite

118

125

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“…Two important peripheral signals are leptin, the product of the obesity (Ob) gene, which is secreted mainly from adipocytes, and insulin, produced mainly in the pancreas, which also signals energy status to the hypothalamus (Zhang et al 1994, Niswender & Schwartz 2003. Leptin and insulin modulate neurons within the arcuate nucleus and are thought to act through their specific receptors on melanocortin neurons (Niswender & Schwartz 2003, Breen et al 2005. The two main opposing neurons in the melanocortin system express either the orexigenic hormones, NPY and AgRP, or the anorexigenic hormones, proopiomelanocortin (POMC) and cocaine and amphetamine-regulated transcript (CART).…”

Section: Introductionmentioning

confidence: 99%

Glucose regulates AMP-activated protein kinase activity and gene expression in clonal, hypothalamic neurons expressing proopiomelanocortin: additive effects of leptin or insulin

Cai¹,

Gyulkhandanyan²,

Wheeler³

et al. 2007

Journal of Endocrinology

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The mammalian hypothalamus comprises an array of phenotypically distinct cell types that interpret peripheral signals of energy status and, in turn, elicits an appropriate response to maintain energy homeostasis. We used a clonal representative hypothalamic cell model expressing proopiomelanocortin (POMC; N-43/5) to study changes in AMPactivated protein kinase (AMPK) activity and glucose responsiveness. We have demonstrated the presence of cellular machinery responsible for glucose sensing in the cell line, including glucokinase, glucose transporters, and appropriate ion channels. ATP-sensitive potassium channels were functional and responded to glucose. The N-43/5 POMC neurons may therefore be an appropriate cell model to study glucose-sensing mechanisms in the hypothalamus. In N-43/5 POMC neurons, increasing glucose concentrations decreased phospho-AMPK activity. As a relevant downstream effect, we found that POMC transcription increased with 2 . 8 and 16 . 7 mM glucose. Upon addition of leptin, with either no glucose or with 5 mM glucose, we found that leptin decreased AMPK activity in N-43/5 POMC neurons, but had no significant effect at 25 mM glucose, whereas insulin decreased AMPK activity at only 5 mM glucose. These results demonstrate that individual hypothalamic neuronal cell types, such as the POMC neuron, can have distinct responses to peripheral signals that relay energy status to the brain, and will therefore be activated uniquely to control neuroendocrine function.

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“…In addition, feeding state alters both POMC neuron activity in terms of c-Fos induction (Elias et al, 1999;Shu et al, 2003) and POMC peptide release (Dube et al, 2000;Breen et al, 2005). Feeding state also affects the levels of endocannabinoids in the hypothalamus (Di Marzo et al, 2001;Kirkham et al, 2002).…”

Section: Introductionmentioning

confidence: 99%