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Deficiency of polyunsaturated fatty acids (PUFAs) is known to induce hepatic steatosis. However, it is not clearly understood which type of PUFA is responsible for the worsening of steatosis. This study observed a marked accumulation of hepatic triacylglycerol and cholesterol in fatty acid desaturase 2 knockout (FADS2−/−) mice lacking both C18 and ≥ C20 PUFAs that were fed a PUFA‐depleted diet. Hepatic triacylglycerol accumulation was associated with enhanced sterol regulatory element‐binding protein (SREBP)‐1‐dependent lipogenesis and decreased triacylglycerol secretion into the plasma via very‐low‐density lipoprotein (VLDL). Furthermore, upregulation of cholesterol synthesis contributed to increased hepatic cholesterol content in FADS2−/− mice. These results suggest that ≥ C20 PUFAs synthesized by FADS2 are important in regulating hepatic triacylglycerol and cholesterol accumulation during PUFA deficiency. [ABSTRACT FROM AUTHOR]

Fatty acid‐binding protein (FABP) 5 is highly expressed in various types of tumors and is strongly correlated with tumor growth, development, and metastasis. However, it is unclear how the expression of FABP5 in the host affects tumor progression. In this study, using a lung tumor metastasis model in mice, we found that FABP5‐deficient mice were more susceptible to tumor metastasis, which is accompanied by infiltration of a lower frequency of activated natural killer (NK) cells in the lung. Additionally, FABP5 deficiency leads to impaired maturation of NK cells in the lungs, but not in the bone marrow and spleen. Taken together, our results provide the first evidence that FABP5 in the host regulates lung tumor metastasis through controlling NK cell maturation. [ABSTRACT FROM AUTHOR]

Transient receptor potential vanilloid subfamily 1 (TRPV1) is a non‐selective cation channel protein expressed in neuronal and non‐neuronal cells. Although TRPV1 is implicated in thermogenesis and diet‐induced obesity (DIO), its precise role remains controversial. TRPV1−/− mice are protected from DIO, while TRPV1 activation enhances thermogenesis to prevent obesity. To reconcile this, we fed wild‐type and TRPV1−/− mice for 32 weeks with normal chow or a high‐fat diet and analyzed the weight gain, metabolic activities, and thermogenic protein expression in white and brown fats. TRPV1−/− mice became obese, exhibited reduced locomotor activity, reduced energy expenditure, enhanced hepatic steatosis, and decreased thermogenic protein expression in adipose tissues. Our data reveal that lack of TRPV1 does not prevent obesity, but rather enhances metabolic dysfunction. [ABSTRACT FROM AUTHOR]