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In recent decades, the consumption of fructose in Western societies has surged to unprecedented levels, primarily driven by agricultural and industrial advancements in the production of sweeteners such as sucrose and high-fructose corn syrup (HFCS). This increased fructose intake has contributed significantly to the escalating prevalence of obesity and associated metabolic diseases, such as type 2 diabetes (T2D) and metabolic dysfunction-associated steatotic liver disease (MASLD).

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Endothelial autophagy-related gene 7 contributes to high fat diet-induced obesity

Guang Ren, Sushant Bhatnagar, Martin E. Young, Timmy Lee, Jeong-a Kim

Endothelial autophagy-related gene 7 contributes to high fat diet-induced obesity

 

Objective

Obesity-associated metabolic dysfunction is a major public health concern worldwide. Endothelial dysfunction is a hallmark of metabolic dysfunction, and endothelial cells affect metabolic functions. Because autophagy-related gene 7 (ATG7) is involved in various cellular physiology, we investigated the roles of endothelial cell-ATG7 (EC-ATG7) on high-fat diet-induced obesity and its related metabolic dysfunction.

Methods

We generated an endothelial-specific Atg7 knock-out mouse by breeding Atg7flox/flox mouse with the Chd5-Cre mouse, and investigated the metabolic phenotypes associated with high-fat diet (HFD)-induced obesity. Body weight, food intake, glucose tolerance, insulin sensitivity, and liver fat accumulation were measured in endothelial Atg7 deficient (Atg7ΔEnd) and control mice (Atg7f/f). Adipose tissue inflammation was assessed by measuring the expression of pro-inflammatory genes. Furthermore, we performed indirect calorimetry and examined the insulin signaling pathway molecules.

Results

We found that deletion of EC-Atg7 ameliorated HFD-induced weight gain, fatty liver, and adipocyte hypertrophy and inflammatory response in adipose tissue, and improved insulin sensitivity without changing glucose tolerance. These metabolic effects seem to be due to the reduced food intake because there were no differences in energy expenditure, energy excretion to feces, and physical activity. Interestingly, the deletion of EC-Atg7 protected from HFD-induced vascular rarefaction, and the knock-down of Atg7 in endothelial cells protected from fatty acid-induced cell death.

Conclusions

Our results suggest that EC-Atg7 deletion ameliorates HFD-induced obesity and its related metabolic dysfunction, such as insulin resistance and fatty liver by attenuating appetite and vascular rarefaction. The EC-Atg7 deletion may protect the endothelial cells from lipotoxicity and impaired angiogenesis, which preserves the endothelial function in metabolic tissues. These findings may have implications for developing new therapeutic strategies for preventing and treating obesity and its associated health risks.

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Articles in Press

Endothelial autophagy-related gene 7 contributes to high fat diet-induced obesity

Guang Ren, Sushant Bhatnagar, Martin E. Young, Timmy Lee, Jeong-a Kim

Endothelial autophagy-related gene 7 contributes to high fat diet-induced obesity

 

Objective

Obesity-associated metabolic dysfunction is a major public health concern worldwide. Endothelial dysfunction is a hallmark of metabolic dysfunction, and endothelial cells affect metabolic functions. Because autophagy-related gene 7 (ATG7) is involved in various cellular physiology, we investigated the roles of endothelial cell-ATG7 (EC-ATG7) on high-fat diet-induced obesity and its related metabolic dysfunction.

Methods

We generated an endothelial-specific Atg7 knock-out mouse by breeding Atg7flox/flox mouse with the Chd5-Cre mouse, and investigated the metabolic phenotypes associated with high-fat diet (HFD)-induced obesity. Body weight, food intake, glucose tolerance, insulin sensitivity, and liver fat accumulation were measured in endothelial Atg7 deficient (Atg7ΔEnd) and control mice (Atg7f/f). Adipose tissue inflammation was assessed by measuring the expression of pro-inflammatory genes. Furthermore, we performed indirect calorimetry and examined the insulin signaling pathway molecules.

Results

We found that deletion of EC-Atg7 ameliorated HFD-induced weight gain, fatty liver, and adipocyte hypertrophy and inflammatory response in adipose tissue, and improved insulin sensitivity without changing glucose tolerance. These metabolic effects seem to be due to the reduced food intake because there were no differences in energy expenditure, energy excretion to feces, and physical activity. Interestingly, the deletion of EC-Atg7 protected from HFD-induced vascular rarefaction, and the knock-down of Atg7 in endothelial cells protected from fatty acid-induced cell death.

Conclusions

Our results suggest that EC-Atg7 deletion ameliorates HFD-induced obesity and its related metabolic dysfunction, such as insulin resistance and fatty liver by attenuating appetite and vascular rarefaction. The EC-Atg7 deletion may protect the endothelial cells from lipotoxicity and impaired angiogenesis, which preserves the endothelial function in metabolic tissues. These findings may have implications for developing new therapeutic strategies for preventing and treating obesity and its associated health risks.

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12th Helmholtz 
Diabetes Conference 
22-24. Sep, Munich

You are what you eat

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