Type 2 diabetes results in chronic diseases, including diabetic nephropathy (disease related to the kidney), diabetic retinopathy (disease related to eyes), and diabetic neuropathy (nontraumatic lower-limb amputations). Due to continuous changes in the eating behavior and activity level of human beings, the incidence of type 2 diabetes is increasing continuously
[5]. The disease results due to impaired secretion and resistance of insulin inside the body. The major risk effect for insulin resistance is obesity, and a strong relationship between these two factors has been reported in both animal and human studies
[6]. Therefore, improvements in obesity result in the improvement of insulin sensitivity and the prevention of type 2 diabetes. Ternatin is a highly methylated cyclic heptapeptide.
This compound inhibits the effect of fat accumulation, which was studied using 3T3-L1 adipocytes
[7]. According to
Figure 2, ternatin reduced the mRNA levels of CCAAT/enhancer-binding protein-a (C/EBP-a and sterol regulatory element-binding protein-1c (SREBP-1c)) at an early stage of differentiation in preadipocytes; this results in the suppression of peroxisome proliferative-activated receptors c (PPAR-cmRNA)
[8]. The suppression results in the reduction of messenger RNA levels of adipocyte fatty acid-binding protein (aP2), lipoprotein lipase, FAS (fatty acid synthase), and ACC2 (acetyl-CoA carboxylase) due to the cellular lipid accumulation becoming reduced
[9]. The consumption of ternatin also reduced triglyceride synthesis, but its effectiveness is lower in the differentiation of adipocytes than observed in preadipocytes. D-Leu7 is a derivative of ternatin that is demonstrated to inhibit the accumulation of fats in 3T3-L1 cells and is eight times more effective with a 12-fold higher cytotoxic activity (IC
50) than that of ternatin
[10]. Kobayashi et al., in their study, reported that [D-Leu7] ternatin acts by suppressing the expression of lipogenic genes in diabetic Kuo Kondo yellow obese (KK-A(y)) mice and inhibits the accumulation of fats in cultured adipocytes
[11]. They also reported that ternatin and its derivative compound can be a valuable drug for the treatment of obesity. The finding of this study proved that the compound present in mushrooms significantly (
p < 0.05) lowers the glucose and triglycerides. Furthermore, Xian et al. reported the effect of an aqueous extract of mushrooms in improving the insulin resistance with the Pl3K/Akt and p38 MAPK signaling pathways, which are involved in diabetic skeletal muscles
[12]. In their study, they induced insulin-resistant rat models by T2DM with HFD feeding and STZ injection for the manifestation of serious metabolic diseases that exhibit the characteristics of hyperglycemia, hypertension, and dyslipidemia. The insulin-resistant rats in their study displayed certain changes in their bodies that included an increase in venous blood glucose and physiological indexes like the body weight, intake of water, and intake of food. When these rats were treated with mushroom extract in different concentrations of the dosage, the physiological index and glucose level improved compared to the untreated T2DM. In their experiment, it was revealed for the first time that a direct demonstration of the mushroom extract could improve the level of glucose in skeletal muscles. The antiobesity effect of the polysaccharides obtained from
Trametes versicolor was investigated by in vivo methods, and it was observed that the polysaccharides triggered the splenocytes of mice via the MAPK-NF-κB signaling pathway that induced an immunomodulatory effect
[13].