Seipin-calcium ions-mitochondrial metabolism-fat accumulation regulatory pathways.

Adipose tissue is the core of body fat metabolism, and abnormal function can lead to various physiological disorders, which endanger human health.
Seipin gene mutation swells due to severe adipose tissue development and fat storage defects (Lipodystrophy: fat malnutrition) accompanied by non-fat tissue lipid isoteliacaccumulation.
Seipin genes encode nuply-conservative endogenous mesh proteins from yeast and fruit flies to humans, but the molecular function of their proteins and the mechanisms of mutation has not yet been fully clarified.
the Huang Xun Research Group of the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences, based on fruit flies as a model creature, is committed to the study of lipid metabolism regulation.
by establishing a model of fruit fly Seipin mutation, previous studies found that Seipin regulated fat storage in adipose and non-fat tissue by tissue-specificity, and then found that Seipin interacted with the endosconotma calcium ion channel protein SERCA and jointly regulated the calcium ion balance in cells to affect fat storage in adipose tissue.
However, what effect mechanism responds to the calcium signal seiperin/SERCA complex control and mediates fat accumulation.
in the latest research work, Huang Xun's research team carried out the molecular spectrum analysis of the seipin mutant fruit fly adipose tissue at three levels of proteomics, transcription groups, and metablegroups.
integrated comprehensive histological data found that seipin mutants in the glycoenzyme to the mitochondrial triamcinolone circulation of metabolic bottlenecks, resulting in a significant reduction in the raw material (citric acid) content of synthetic fats.
stable isotope marker metabolic flow tracking experiment also confirmed this finding and led the team to further observe the mitochondria of mutant adipose tissue.
study found significant att-by-the-matter deficiencies in Seipin mutant adipose tissue, weakening of mitochondrial breathing levels, increased mitochondrial autophagy, and severe deficiency of mitochondrial calcium ions.
based on the calcium ion balance of the internal cell matrix mediated by the Seipin/SERCA complex found earlier, it is speculated that the lack of mitochondrial calcium ions in the mutant sehast is caused by the lack of calcium ions in the endoscotopal network, which leads to a reduction in the metabolic activity of mitochondrial triamcinolita cyclic acid cycle and insufficient supply of fat synthesis raw materials (citric acid).
the genetic recovery of the calcium ion levels of mitochondria, the addition of citric acid in food or drug intervention to improve the activity of the mitochondria's key metabolic reactions are very good to restore the fat accumulation of mutants.
the study found that the mitochondrial metabolism of calcium ion dependence maintains the steady state of fat cell lipids, reveals the regulatory pathways of Seipin-calcium ion-mitochondrial metabolism-fat accumulation, provides new understanding of the molecular function of the disease-causing gene Seipin and the regulation of body fat metabolism, and also provides a number of potential treatments for fat malnutrition disease, study results July 26 Daily online published in the EMBO Journal, Huang Xun Research Group Ph.D. student Ding Long as the first author of the paper, researcher Huang Xun as the paper's communication author, genetic development institute tax light thick research group, Wang Dong research group and Ding Mei research group to participate in cooperative research, research work by the Chinese Academy of Sciences strategic pilot science and technology special, the Ministry of Science and Technology key research and development program and the National Natural Science Foundation of the fund.
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