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In 1975, Arion and colleagues discovered that hepatocytes release glucose into the bloodstream in response to hypoglycaemia using the glucose-6-phosphatase (G6Pase) system. This system is in the endoplasmic reticulum (ER) and is composed of two functionally linked proteins, a G6P transporter subunit (G6PT) and a catalytic subunit called G6P phosphatase (G6Pase). The G6PT subunit promotes the storage of G6P inside the ER, while G6Pase, which has its catalytic domain in the reticular lumen, hydrolyses G6P to yield free glucose + phosphate. The free glucose stored in the reticular lumen can be transported to the cytosol and from there to the extracellular space in hypoglycaemic conditions by a direct mechanism that has not yet been established, but eventually by glucose transporters (GLUTs).

 

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Current Issue

Sema7A protects against high-fat diet-induced obesity and hepatic steatosis by regulating adipo/lipogenesis

Qiongyu Lu, Ziting Liu, Luyao Zhao, Linru Xu, ... Li Zhu

Sema7A protects against high-fat diet-induced obesity and hepatic steatosis by regulating adipo/lipogenesis

Objective

Obesity and related diseases are becoming a growing risk for public health around the world due to the westernized lifestyle. Sema7A, an axonal guidance molecule, has been known to play a role in neurite growth, bone formation, and immune regulation. Whether Sema7A participates in obesity and metabolic diseases is unknown. As several SNPs in SEMA7A and its receptors were found to correlate with BMI and metabolic parameters in the human population, we investigated the potential role of Sema7A in obesity and hepatic steatosis.

Methods

GWAS and GEPIA database was used to analyze SNPs in SEMA7A and the correlation of Sema7A expression with lipid metabolism related genes. Sema7A−/− mice and recombinant Sema7A (rSema7A) were used to study the role of Sema7A in HFD-induced obesity and hepatic steatosis. Adipose tissue-derived mesenchymal stem cells (ADSCs) were used to examine the role of Sema7A in adipogenesislipogenesis and downstream signaling.

Results

Deletion of Sema7A aggravated HFD-induced obesity. Sema7A deletion enhanced adipogenesis in both subcutaneous and visceral ADSCs, while the addition of rSema7A inhibited adipogenesis of ADSCs and lipogenesis of differentiated mature adipocytes. Sema7A inhibits adipo/lipogenesis potentially through its receptor integrin β1 and downstream FAK signaling. Importantly, administration of rSema7A had protective effects against diet-induced obesity in mice. In addition, deletion of Sema7A led to increased hepatic steatosis and insulin resistance in mice.

Conclusions

Our findings reveal a novel inhibitory role of Sema7A in obesity and hepatic steatosis, providing a potential new therapeutic target for obesity and metabolic diseases.

Articles in Press

Sema7A protects against high-fat diet-induced obesity and hepatic steatosis by regulating adipo/lipogenesis

Qiongyu Lu, Ziting Liu, Luyao Zhao, Linru Xu, ... Li Zhu

Sema7A protects against high-fat diet-induced obesity and hepatic steatosis by regulating adipo/lipogenesis

Objective

Obesity and related diseases are becoming a growing risk for public health around the world due to the westernized lifestyle. Sema7A, an axonal guidance molecule, has been known to play a role in neurite growth, bone formation, and immune regulation. Whether Sema7A participates in obesity and metabolic diseases is unknown. As several SNPs in SEMA7A and its receptors were found to correlate with BMI and metabolic parameters in the human population, we investigated the potential role of Sema7A in obesity and hepatic steatosis.

Methods

GWAS and GEPIA database was used to analyze SNPs in SEMA7A and the correlation of Sema7A expression with lipid metabolism related genes. Sema7A−/− mice and recombinant Sema7A (rSema7A) were used to study the role of Sema7A in HFD-induced obesity and hepatic steatosis. Adipose tissue-derived mesenchymal stem cells (ADSCs) were used to examine the role of Sema7A in adipogenesislipogenesis and downstream signaling.

Results

Deletion of Sema7A aggravated HFD-induced obesity. Sema7A deletion enhanced adipogenesis in both subcutaneous and visceral ADSCs, while the addition of rSema7A inhibited adipogenesis of ADSCs and lipogenesis of differentiated mature adipocytes. Sema7A inhibits adipo/lipogenesis potentially through its receptor integrin β1 and downstream FAK signaling. Importantly, administration of rSema7A had protective effects against diet-induced obesity in mice. In addition, deletion of Sema7A led to increased hepatic steatosis and insulin resistance in mice.

Conclusions

Our findings reveal a novel inhibitory role of Sema7A in obesity and hepatic steatosis, providing a potential new therapeutic target for obesity and metabolic diseases.

2021 impact factor: 8.568

You are what you eat

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