## 4 Discussion
Specifically, the organic substance MDA is a by-product of polyunsaturated fatty acids that are present in free radicals. It is closely related to oxidative damage to organisms. MDA is typically used as a biomarker of oxidative stress [28]. TNF-\(\alpha\) can gather inflammatory cells and lead to inflammatory cell infiltration, which is the earliest and most important inflammatory mediator [29]. GSP, a glycated albumin (albumin in high glucose environment occurring non-enzymatic glycosylation), is one of the key links in diabetes complications and can lead to a series of pathological changes [30]. INS is produced by beta cells in pancreatic islets, which can regulate the metabolism of carbohydrates by promoting the absorption of, particularly, glucose from the blood into the liver. Glucose production and secretion by the liver is strongly inhibited by high concentrations of insulin in the blood [31]. GC, which is produced by alpha cells in the pancreas, increases the glucose concentration by promoting gluconeogenesis and glycogenolysis [32]. In the present study, Model showed significantly higher indexes than those of Normal; after treatment, L-LF, HK-LF, L-LP, and HK-LP showed significantly lower indexes than those of Model. L-LF (or L-LP) also exhibited significantly decreased indexes relative to those of HK-LF (or HK-LP). Thus, these results showed that LF and LP treatment positively affected the inflammation of the liver and insulin resistance in mice with diabetes and that the live group exerted effects better than those of the heat-killed group. In addition, mice with diabetes were accompanied by insulin resistance and insulin target tissue damage. Thus, we measured the related gene expression level of the liver to further research the mechanism underlying their anti-diabetic effects. IL-1\(\beta\) and TNF-\(\alpha\) are typical pro-inflammatory cytokines. IRS-1 plays a key role in the insulin signaling pathway. GLUT-4, an insulin-regulated glucose transporter, is mainly regulated by the insulin signaling pathway and is the rate-limiting step in glucose metabolism. Thus, evaluating the expression levels of GLUT-4 is important in the study of diabetes [11]. Previous studies indicated that inflammatory factors can affect insulin sensitivity by active insulin signaling, and they can enhance IRS-1 serine phosphorylation and inhabit tyrosine phosphorylation of insulin receptor, then the insulin physiological function and the expression of GLUT-4 were reduced. Finally, the insulin stimulation and glucose transport function were weakened [33]. PPAR\(\gamma\) mainly mediates inflammation, lipid metabolism, and the maintenance of metabolic homeostasis [34]. SREBP-1c is associated with glucose metabolism as well as fatty acid and lipid production, and its expression is regulated by insulin [35]. In the current study, we demonstrated that the expression levels of IL-1\(\beta\) and TNF-\(\alpha\) were significantly decreased and that the expression levels of IRS-1, GLUT-4, SREBP-1c, and PPAR\(\gamma\) were significantly increased in treated LF and LP. The regulating effects of the live group were more apparent than those of the heat-killed group. Therefore, LF and LP play an important role in preventing inflammation of the liver and hepatic insulin resistance in mice with diabetes induced by a high-fat diet combined with STZ. The preventive effects of the corresponding live group were better than those of the heat-killed group. However, other problems have yet to be addressed. First, the regulating mechanisms of LF and LP to diabetes remain unclear, so that their mechanisms need to be further defined. This study can provide basic theories for their functional application. Second, the live and heat-killed LF and LP can play an efficient role in preventing diabetes; however, a difference still exists. The reason for this difference needs to be identified, and the cellular components of LF and LP exhibiting these special properties need to be determined.