Key result
PLAAT1 deficiency in mice resulted in lower body weight gain, reduced liver weight, and negligible hepatic lipid accumulation compared to wild-type mice on a high-fat diet.
Why the study?
Plaat3-deficient mice show hepatic fat accumulation under high-fat diet feeding, but Plaat1-deficient mice had not been analyzed.
Does PLAAT1 deficiency reduce high-fat diet-induced obesity and hepatic lipid accumulation in mice?
Does PLAAT1 deficiency reduce high-fat diet-induced obesity and hepatic lipid accumulation in mice?
PLAAT1 deficiency protects against high-fat diet-induced obesity and hepatic steatosis in mice without increasing insulin resistance.
Suggests PLAAT1 as a target in metabolic liver disease; extends preclinical models but leaves open human translation.
The phospholipase A and acyltransferase (PLAAT) family is composed of three isoforms in mice (PLAAT1, 3, and 5), all of which function as phospholipid‐metabolizing enzymes exhibiting phospholipase A 1 /A 2 and acyltransferase activities. Plaat3 ‐deficient ( Plaat3 −/− ) mice were previously reported to show lean phenotype and remarkable hepatic fat accumulation under high‐fat diet (HFD) feeding, while Plaat1 −/− mice have not been analyzed. In the present study, we generated Plaat1 −/− mice and investigated the effects of PLAAT1 deficiency on HFD‐induced obesity, hepatic lipid accumulation, and insulin resistance. After HFD treatment, PLAAT1 deficiency caused a lower body weight gain compared to wild‐type mice. Plaat1 −/− mice also showed reduced liver weight with negligible hepatic lipid accumulation. In accordance with these findings, PLAAT1 deficiency improved HFD‐induced hepatic dysfunction and lipid metabolism disorders. Lipidomics analysis in the liver revealed that in Plaat1 −/− mice, the levels of various glycerophospholipids tended to increase, while all classes of lysophospholipids examined tended to decrease, suggesting that PLAAT1 functions as phospholipase A 1 /A 2 in the liver. Interestingly, the HFD treatment of wild‐type mice significantly increased the mRNA level of PLAAT1 in the liver. Furthermore, the deficiency did not appear to elevate the risk of insulin resistance in contrast to PLAAT3 deficiency. These results suggested that the suppression of PLAAT1 improves HFD‐induced overweight and concomitant hepatic lipid accumulation.
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Rahman et al. (2023) studied High-fat diet-induced obesity and hepatic lipid accumulation. PLAAT1 deficiency (Plaat1-/-) vs. Wild-type mice was evaluated on Body weight gain and hepatic lipid accumulation. PLAAT1 deficiency in mice resulted in lower body weight gain, reduced liver weight, and negligible hepatic lipid accumulation compared to wild-type mice on a high-fat diet.
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