Format

Send to

Choose Destination
Br J Nutr. 2007 Oct;98(4):720-6. Epub 2007 Aug 1.

Dietary chickpeas reverse visceral adiposity, dyslipidaemia and insulin resistance in rats induced by a chronic high-fat diet.

Author information

1
Shanghai Institute of Endocrine and Metabolic Diseases, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, 197 Ruijin Road II, Shanghai 200025, China.

Abstract

The improved effects of dietary chickpeas on visceral adiposity, dyslipidaemia and insulin resistance were examined. Rats were fed a normal-fat diet (NFD), a high-fat diet (HFD) or a high-fat plus chickpea diet (HFD+CP) for 8 months. The epididymal fat pad weight v. total body weight of rats was higher in the HFD group (0.032 (sd 0.0042) g/g) than in the NFD group (0.015 (sd 0.0064) g/g) and smaller in the HFD+CP group (0.023 (sd 0.0072) g/g) compared with the HFD group (P < 0.05). Chickpea treatment also induced a favourable plasma lipid profile reflecting decreased TAG, LDL-cholesterol (LDL-C) and LDL-C:HDL-cholesterol levels (P < 0.05). HFD-fed rats had higher TAG concentration in muscle and liver, whereas the addition of chickpeas to the HFD drastically lowered TAG concentration (muscle, 39 %; liver, 23 %). The activities of lipoprotein lipase (LPL) in epididymal adipose tissue and hepatic TAG lipase in liver recorded a 40 and 23 % increase respectively in HFD rats compared with those in NFD rats; dietary chickpeas completely normalised the levels. Furthermore, chickpea-treated obese rats also showed a markedly lower leptin and LPL mRNA content in epididymal adipose tissue. An insulin tolerance test, oral glucose tolerance test and insulin-releasing test showed that chickpeas significantly improved insulin resistance, and prevented postprandial hyperglycaemia and hyperinsulinaemia induced by the chronic HFD. The present findings provide a rational basis for the consumption of chickpeas as a functional food ingredient, which may be beneficial for correcting dyslipidaemia and preventing diabetes.

PMID:
17666145
DOI:
10.1017/S0007114507750870
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Cambridge University Press
Loading ...
Support Center