In our research, SEPT7-deficient mice on HFD showed positive results on GTT rather than ITT (Figure 4A–H), meaning adipocyte SEPT7-deficiency most likely altered mice's capacity on glucose handling and insulin secretion while their insulin sensitivity or counter-regulatory hormone function were left untouched, which can be observed in metabolic syndrome in some cases [56]. This evidence concerns the gene SEPTIN7 and metabolic syndrome.