Previous studies have proposed that overexpression of CD36, GGPPS, PTP-1B, GRK2, and adipose triglyceride lipase may contribute to the development of metabolic syndrome, and Pueraria could eliminate the metabolic adverse effects.
Pro-inflammatory cytokines related to insulin resistance and MetS in children are tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, IL-1β, interferon gamma, pigment epithelium-derived factor, chemerin, vaspin, and fetuin A. Anti-inflammatory cytokines associated with insulin resistance and MetS in children are leptin, adiponectin, omentin, fibroblast growth factor (FGF)-21, osteocalcin, and irisin.
Adipose triglyceride lipase and hormone-sensitive lipase protein expression in subcutaneous adipose tissue is decreased after an isoenergetic low-fat high-complex carbohydrate diet in the metabolic syndrome.
These results complement previous findings of functional studies in mammals and elucidate a potential role of ATGL in pathways involved in components of the metabolic syndrome.