The effects of Enzamin on obesity-related metabolic disorders in obese db/db mice were
examined to explore a novel agent for the prevention of insulin resistance. Db/db mice
were treated with water containing Enzamin (0·1 and 1·0 %) for 8 weeks from 6 weeks of
age. Enzamin treatment at 1·0 %, but not at 0·1 %, significantly decreased the fasting
plasma glucose, serum total cholesterol and TAG levels in db/db mice, without affecting
body weight gain and body fat composition. Furthermore, insulin sensitivity and glucose
tolerance were improved by the treatment of db/db mice with 1·0 % Enzamin.
Immunohistochemical studies and gene expression analysis showed that 1·0 % Enzamin
treatment suppressed macrophage accumulation and inflammation in the adipose tissue. In
addition, 1·0 % Enzamin treatment increased serum adiponectin in db/db mice. Treatment
with 1·0 % Enzamin also significantly suppressed the expression of NADPH oxidase subunits,
suggesting an antioxidative effect for Enzamin in the adipose tissue. Furthermore,
in vitro experiments demonstrated that the lipopolysaccharide-induced
inflammatory reaction was significantly suppressed by Enzamin treatment in macrophages.
Enzamin treatment increased the expression of GLUT4 mRNA in muscle, but not GLUT2 mRNA in
the liver of db/db mice. Enzamin also increased the mRNA expression of carnitine
palmitoyltransferase 1a (CPT1a, muscle isoform) in db/db mice, whereas Enzamin treatment
did not affect the mRNA expression of CPT1b (liver isoform) in db/db mice. In conclusion,
our data indicate that Enzamin can improve insulin resistance by ameliorating impaired
adipocytokine expression, presumably through its anti-inflammatory action, and that
Enzamin possesses a potential for preventing the metabolic syndrome.