Effects of konjac extract on insulin sensitivity in high fat diet rats.
Abstract
AIM: To evaluate the effects of konjac extract (KE) on insulin sensitivity in
insulin resistance (IR) rats induced by high fat diet (HFD).
METHODS: Wistar rats were fed on HFD for 4 weeks, then treated with KE 1.5, 3.0
g/kg/d and metformin (Met) 0.1 g/kg/d for 4 weeks, respectively. The effects of
KE on intake of food and drink, body weight, and excretion were investigated.
Serum insulin was measured by double-radioimmunoassay. Blood glucose, total
cholesterol (TC), triglycerides (TG), and high-density lipoprotein-cholesterol
(HDL-C) were measured by enzyme methods, respectively. Low-density
lipoprotein-cholesterol (LDL-C) was calculated. Tissue glycogen was determined by
modified anthracene ketone method and tissue TG by glycerin phosphor sour
oxidation enzyme method. Insulin sensitivity was measured by modified
glucose-insulin tolerance test (K value).
RESULTS: HFD caused IR after 4 weeks (K value: 5.2+/-0.9 vs 8.3+/-0.7, P<0.01),
the levels of blood insulin, TG, and LDL-C increased, while HDL-C, glycogen in
liver and skeletal muscle decreased. The storage of TG in liver and skeletal
muscle increased. After HFD rats were treated with KE 1.5 and 3.0 g/kg/d for 4
weeks, respectively, the fasting blood glucose (FBG) was decreased from 6.4+/-0.4
to 6.05+/-0.26, 6.0+/-0.3 (P<0.01). Serum TC, TG, LDL-C were decreased, while
HDL-C/TC was increased as compared with HFD rats. There was no significant effect
on insulin level. KE 1.5, 3.0 g/kg/d, and Met 0.1 g/kg/d could improve insulin
sensitivity (K values were 6.1+/-0.5, 5.9+/-0.6, and 6.5+/-0.8 vs 5.2+/-0.9,
P<0.05), elevate glycogen, and decrease TG in liver and skeletal muscle.
CONCLUSION: KE could promote glycogen syntheses and adjust blood lipid metabolism
so as to improve IR in HFD rats.
Keywords:
insulin resistance (IR) rats induced by high fat diet (HFD).
METHODS: Wistar rats were fed on HFD for 4 weeks, then treated with KE 1.5, 3.0
g/kg/d and metformin (Met) 0.1 g/kg/d for 4 weeks, respectively. The effects of
KE on intake of food and drink, body weight, and excretion were investigated.
Serum insulin was measured by double-radioimmunoassay. Blood glucose, total
cholesterol (TC), triglycerides (TG), and high-density lipoprotein-cholesterol
(HDL-C) were measured by enzyme methods, respectively. Low-density
lipoprotein-cholesterol (LDL-C) was calculated. Tissue glycogen was determined by
modified anthracene ketone method and tissue TG by glycerin phosphor sour
oxidation enzyme method. Insulin sensitivity was measured by modified
glucose-insulin tolerance test (K value).
RESULTS: HFD caused IR after 4 weeks (K value: 5.2+/-0.9 vs 8.3+/-0.7, P<0.01),
the levels of blood insulin, TG, and LDL-C increased, while HDL-C, glycogen in
liver and skeletal muscle decreased. The storage of TG in liver and skeletal
muscle increased. After HFD rats were treated with KE 1.5 and 3.0 g/kg/d for 4
weeks, respectively, the fasting blood glucose (FBG) was decreased from 6.4+/-0.4
to 6.05+/-0.26, 6.0+/-0.3 (P<0.01). Serum TC, TG, LDL-C were decreased, while
HDL-C/TC was increased as compared with HFD rats. There was no significant effect
on insulin level. KE 1.5, 3.0 g/kg/d, and Met 0.1 g/kg/d could improve insulin
sensitivity (K values were 6.1+/-0.5, 5.9+/-0.6, and 6.5+/-0.8 vs 5.2+/-0.9,
P<0.05), elevate glycogen, and decrease TG in liver and skeletal muscle.
CONCLUSION: KE could promote glycogen syntheses and adjust blood lipid metabolism
so as to improve IR in HFD rats.