[Lotus]

So the hypothalamus has been holding out on us, it turns out it controls appetite too, that sneaky thing.

Obesity results from an imbalance between energy intake and energy expenditure. The brain is an integral regulator of energy intake and energy expenditure, and thus whole-body energy homeostasis. The hypothalamus is important to the central regulation of energy homeostasis in the hypothalamic ARC control of food intake and regulation of energy balance, the mechanism(s) by which this occurs has not been established. Malonyl CoA inhibits carnitine palmitoyltransferase-1 (CPT-1), and it has been proposed that the substrate of CPT-1, long-chain acyl CoA(s), may act as a mediator(s) of appetite and energy balance.
Targeting Intermediary Metabolism in the Hypothalamus as a Mechanism to Regulate Appetite
http://pharmrev.aspetjournals.org/conten...7.full.pdf

In particular, inhibiting FAS (fatty acids synthase) suppresses appetite via an increase malonyl CoA, exactly where do we find malonyl CoA???.......it's in leptin (or shall we say the release of leptin).

Leptin, an anorexigenic hormone secreted from adipocytes, can increase malonyl CoA levels in the ARC by activating ACC (Gao et al., 2007b). Recent evidence suggests that this up-regulation of malonyl CoA in the ARC mediates the anorectic signaling actions of leptin (Gao et al., 2007b

The inhibition of FAS has been attributed to an increase of malonyl CoA levels in the hypothalamus (Hu et al., 2003), which subsequently is linked to an increase of fatty acid oxidation rates in skeletal muscle (Cha et al., 2005, 2006)

Hypothalamic malonyl-CoA and the control of food intake.
Gao S, et al. Physiol Behav. 2013.

Abstract
Fatty acid metabolism is implicated in the hypothalamic control of food intake. In this regard, malonyl-CoA, an intermediate in fatty acid synthesis, is emerging as a key player. Malonyl-CoA in the hypothalamus has been proposed as an anorectic mediator in the central control of feeding. A large body of evidence demonstrates that modulating hypothalamic activities of malonyl-CoA metabolic enzymes impacts food intake. Malonyl-CoA action appears to play a significant role in the intracellular signaling pathways underlying leptin anorectic effect in the arcuate nucleus. Ghrelin's hypothalamic effect on feeding may also involve the change in malonyl-CoA metabolism. Hypothalamic malonyl-CoA levels are altered in response to fasting and refeeding, suggesting physiological relevance of the changes in malonyl-CoA level in the controls of feeding and energy balance. -CoA inhibits the acyltransferase activity of carnitine palmitoyltransferase-1 (CPT-1), and CPT-1 was considered as a downstream effector in hypothalamic malonyl-CoA effect on feeding. However, recent evidence has not been entirely consistent with this notion. In the arcuate nucleus, the inhibition of CPT-1 acyltransferase activity does not play an important role in the feeding effect of either leptin or cerulenin (a fatty acid synthase inhibitor) that requires the increase in malonyl-CoA level. Alternatively, the brain isoform of CPT-1 (CPT-1c) may act as a downstream target in the malonyl-CoA signaling pathways. CPT-1c does not possess a typical acyltransferase activity, and the exact molecular function of this protein is currently unknown. Recent data indicate it is involved in ceramide metabolism. Of relevance, in the arcuate nucleus, CPT-1c may link malonyl-CoA to ceramide metabolism to affect food intake.

© 2013. PMID 23988346 [PubMed - indexed for MEDLINE] PMCID PMC4803278


So.......what does this mean for NBE?, imo.....the release of leptin can inhibit appetite and oh btw release aromatase. Say what!!!!

the hypothalamus contains several contains several clusters of neurons, commonly designated as nuclei. Current research indicates that one of these, the arcuate nucleus, houses the appetite center.

Appetite, Metabolism and Obesity
http://www.medbio.info/Horn/PDF%20files/...02013a.pdf