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Recent studies revealed that high levels of VAT Tregs in female mice protected the mice from high fat diet (HFD -induced metabolic disorders compared witHFD -induced
In a recent study, Feige et al. [ 16] even found that the phthalate protected wild-type C57BL/6 mice from high fat diet-induced body weight increases.
Though the precise mechanism is not clear, it has been shown that adipose VEGF expression protects mice from high fat diet-induced obesity, glucose intolerance, insulin resistance, and adipose tissue inflammation.
Moreover, overexpression of COX-2 in WAT of mice effectively induces de novo recruitment of brown adipocytes, elevates the energy expenditure of mice and protects the mice from high fat diet induced obesity.
In mammals, deletion of the homolog of Indy (mIndy, Slc13A5), protects mice from high fat diet and aging induced obesity, insulin resistance and nonalcoholic fatty liver disease (NAFLD), at least in part through the activation of the intracellular energy sensor AMP-activated protein kinase A (AMPK) [ 6].
They showed that PGRN expression was induced by TNF- α or dexamethasone and decreased with differentiation of adipocytes, and ablation of PGRN prevented mice from high fat diet-induced insulin resistance and blocked elevation of an inflammatory cytokine, IL-6, in adipose tissue [ 26].
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Liu, C. et al. Targeting arginase-II protects mice from high-fat-diet-induced hepatic steatosis through suppression of macrophage inflammation.
Inactivation of Ces1d protected mice from high-fat diet induced steatosis.
Moreover, the loss of CaMKK2 protects mice from high-fat diet-induced obesity, insulin resistance, and glucose intolerance.
The loss of Slc13a5 also protects mice from high-fat diet induced obesity and insulin resistance (Birkenfeld et al., 2011).
These effects can protect mice from high-fat (HF -induced metabolic disease (Cantó et al., 2012).
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