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Aging is a growing trend in modern societies, and the incidence of aging-related obesity has been on a steady rise. The key cause of obesity of older adults is identified as the decreased lipolysis of adipocytes, which in turn can be attributed to the decreased expression of key lipases in senescent adipocytes, but effective clinical measures to enhance the lipase expression are currently lacking. In this work, we studied the influence of the total saponins from Panax japonicus (TSPJs) on the expression of key lipases in senescent adipocytes, which can provide an experimental basis for potentially using TSPJs to address aging-related obesity. We found that TSPJs could regulate lipase expression through the ALK7-SMADs signaling pathway, to restore the lipase expression in senescent adipocytes and thus improve lipolysis.

Aging and obesity are closely related. A key change in the adipose tissue during the aging process is the decline of lipolysis. The excitation of the sympathetic nerve system is a key pathway to promote lipolysis, but the underlying mechanism remains unclear. In this work, in vitro and in vivo aging models with and without tyrosine hydroxylase (TH) knockdown were treated with total saponins from Panax japonicus (TSPJs), and the expression of lipolysis-related proteins was examined. It was found that TSPJs could promote the expression of lipolysis-related genes and TH in adipocytes both in vitro and in vivo, and the expression of lipolysis-related genes was downregulated after TH knockdown. It was inferred that TSPJs could promote the excitation of sympathetic nerves by increasing the expression of TH in adipose tissue, which positively regulated the expression of lipases to revitalize lipolysis. The results suggested that TSPJs resisted aging-induced obesity and could be a potential medication for weight management.

Our prophase studies have manifested that the sweet triterpenoid glycoside from the leaves of Cyclocarya paliurus (CPST) effectively improved the disorders of glucolipid metabolism in vitro and in patients. The current purpose was to further detect its mechanisms involved. The results demonstrated that CPST could ameliorate high-fat diet (HFD)-induced insulin resistance (IR), which was linked to reducing HFD-induced mice's body weight, serum glucose (GLUO), triglyceride (TG), total cholesterol (T-CHO) and low-density lipoprotein cholesterol (LDL-C), lowering the area under the oral glucose tolerance curve and insulin tolerance, elevating the percentage of brown adipose, high-density lipoprotein cholesterol (HDL-C), reducing fat droplets of adipocytes in interscapular brown adipose tissue (iBAT) and cross-sectional area of adipocytes. Further studies manifested that CPST obviously downregulated TLR4, MyD88, NLRP3, ASC, caspase-1, cleased-caspase-1, IL-18, IL-1β, TXNIP, and GSDMD protein expressions and p-NF-кB/NF-кB ratio in iBAT. These aforementioned findings demonstrated that CPST ameliorated HFD induced IR by regulating TLR4/NF-κB/NLRP3 signaling pathway, which in turn enhancing insulin sensitivity and glucose metabolism.