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The FLT4 gene plays an important role in the onset and progression of obesity and is involved in the structure and function of lymphatic vessels. By inducing a mouse obesity model with a high-fat diet and knocking out the FLT4 gene, which is associated with lymphatic vessel growth in mice, FLT4+/− mice were found to be susceptible to high-fat diet-induced obesity, with significant accumulation of visceral fat. BODIPY™ FL C 16 imaging revealed dilated and branched mesenteric lymphatic vessels in FLT4+/− mice. Immunofluorescence staining showed that FLT4+/− exacerbated the morphological abnormalities of lymphatic vessels and submucosal lymphatic vessels in visceral adipose tissue of obese mice, accompanied by macrophage infiltration around lymphatic vessels. In addition, FLT4 knock down increased the proportion of M1-type macrophages in the adipose tissue of the epididymis, indicating significant chronic inflammation in FLT4+/− obese mice. These findings provide new evidence for the involvement of lymphatic vessel morphological abnormalities in the onset and progression of obesity and highlight the importance of further investigation of FLT4 to better understand the mechanism of HFD-induced obesity and to develop related treatments. • Wild-type hyper-fat mice were obese and developed mesenteric lymphangiectasia. • On a high-fat diet, FLT4+/− mice gained more weight and developed abnormal glucose tolerance than wild-type mice. • In obese FLT4+/− mice, fat accumulated in the mesentery, and lymphatic vessels increased in diameter and branching. • Obese FLT4+/- mice showed macrophage accumulation around mesenteric and epididymal adipose tissue lymphatic vessels. [ABSTRACT FROM AUTHOR]