PNAS: E-Syt3 in hypothyclycertic POMC neurons played an important role in the formation of nutritional obesity.

In recent years, obesity has increased rapidly in both developed and developing countries.
obesity can cause or promote cardiovascular disease, type 2 diabetes, and non-alcoholic fatty liver diseases that harm human health, it is important to study the causes of obesity formation to develop new treatments.
at the base of the brain is the central body that regulates the body's energy metabolism.
the neurons of proopiomelanocortin (POMC) in the arch nucleus (Arc) have an important role in the regulation of energy balance.
activate POMC neurons to suppress appetite and promote heat production in the body.
POMC presupposor peptides are processed to form mature peptides, such as alpha-Melanocyte-active hormone, alpha-MSH, which act on neurons outside the hypothyroid and hypothyroids, thereby suppressing appetite and increasing heat production.
recently, Professor Zhang Guo of Hua zhong University of Science and Technology, Professor Cai Dongsheng of Einstein College of Medicine and Professor Li Ju of Nanjing Medical University published a paper entitled Hypothalamic Extended synaptotagmin-3 contributes to the development of the development of the University of Science and Technology in PNAS. The research paper on obesity and related metabolic disorders reveals the role of Extended synaptotagmin-3 (E-Syt3) in the formation of diet-induced obesity (DIO) in hyalural neurons.
E-Syt protein, which binds to Ca2 plus, is a sub-family of C2-containing domain proteins.
E-Syt evolved into a highly conservative protein subgeneration, found in a wide range of organisms, from plants and yeast to mammals.
in mammalian cells, the E-Syt protein subgeneration consists of three members: E-Syt1, E-Syt2, and E-Syt3.
previous studies have shown that E-Syt proteins are able to mediate contact between endoblasts and membranes and play an important role in intracellular lipid stability.
the E-Syt gene in the cell can cause the accumulation of diacylglycerol (DAG) on the mass membrane.
studies have shown that E-Syt3 is expressed in the central nervous system and in some peripheral tissues.
functionally, the researchers looked at E-Syt2 and E-Syt3 double-gene knock-out mice and E-Syt1, E-Syt2, and E-Syt3-knocking mice, but found no significant abnormalities.
histological analysis of two-gene knock-out mice also found no abnormalities in the lungs, spleen, testicles, and muscle tissue.
, little is known about the physiological and/or pathological role of the E-Syt protein.
study, the authors first used histological staining to find that E-Syt3 was expressed in neurons in nuclear groups such as the bow nucleus of the hycthyroid brain.
under high-fat food feeding conditions, body or POMC neuron-specific knockout E-Syt3 inhibits appetite in mice and promotes heat production.
, knocking out the gene could partially alleviate obesity and related combinations caused by eating high-calorie foods, including abnormal sugar tolerance and blood lipids.
contrast, overexposing E-Syt3 in bow-shaped nucleons can, on the other way, promote food intake and reduce heat production, leading to excessive weight gain.
mechanism, the study found that E-Syt3, which is raised in high-calorie foods, had significantly increased levels of alpha-MSH in the hypothyclycerta.
further analysis showed that knocking out the E-Syt3 gene could cause POMC prebiotor peptides to be processed into alpha-MSH. The absence of the
E-Syt3 gene causes the activation of the PKC-AP-1 signaling path, which in turn promotes the transcription activity of the hydrolyzed enzyme PC1/3 and PC2 genes needed to encode POMC polypeptide processing, increases the formation of alpha-MSH;
, the study showed that E-Syt3 in poMC neurons in the hypothyclycertic brain played an important role in the formation of nutritional obesity.
the results suggest the molecule may be a new target for obesity medication.
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