Energy homeostasis plays a
critical role controlling how much we should eat in order to provide sufficient
energy to our bodies. Unfortunately, this system does not always work properly
in any bodies in which it signals the body to intake more food even after a
person just eat five grilled cheese burgers. Consequently, people with this
disorder usually have heavy body weight, or obesity. It is widely believed that
the neural system is responsible for regulating energy homeostasis according to
Bernard and his teams.
Particularly, according to the
article 'Melanocortin-4 receptor-regulated energy homeostasis”, the authors
points out that the central melanocortin system accounts for body weights and overall
metabolic fitness. Within that neural circuit, MC4R neural population is
believed to be the diverging signal although the majority of the population
remains unknown. What captured my attention in this article is that the authors
also found "there is the contribution of MC4Rs in enteroendocrine L-cells
of the intestine which is activated by the release of GLP1 and Peptide YY.
Therefore, potentially enhancing centrally mediated MC4R signaling can improve
the weight loss and the energy expenditure efficacy".
This finding reminds me the
review "Gut-feelings: the emerging biology of gut-brain communication",
Mayer and his collaborators claim that gut microbiota can liberate various
neurotransmitters, such as peptide YY, GLP1 ghrelin, 5-HT, to elicit satiety
and emotional responses. Recently, more and more studies find that microbiota
in the gut can influence our behavior. If this is true, it would provide a
better clinical avenue to treat energy homeostasis disorder because engineered
bacteria are much more targeting than medications.
Link for "Melanocortin-4 receptor-regulated energy homeostasis" :https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5244821/
Link for "Gut-feelings: the emerging biology of gut-brain communication" : https://www.ncbi.nlm.nih.gov/pubmed/21750565
Link for " Body Energy Homeostasis" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605663/
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