As inflammation is considered to be a major factor contributing to type 2 diabetes [68], we examined proinflammatory markers including TNF-α and IL-6 in the serum, and found that GS treatment inhibited serum TNF-α and IL-6 (Table 2), indicating that the anti-inflammatory properties of GS result in protection against insulin resistance, consistent with a previous report [69], revealing that the suppression of inflammation via the modulation of adiponectin, IL-6, and TNF-α is an important protective factor against insulin resistance. This evidence concerns the gene TNF and Insulin resistance.