August 20/Pharma Investments, Ventures & Law Weekly -- According to recent research from the U.S., "The health benefits of pomegranate consumption have recently received considerable scientific focus, with most studies examining fruit and/or juice consumption. Pomegranate seed oil (POMo) is a rich source of 9-cis, 11-trans conjugate linolenic acid (CLA), which may offset the side-effects associated with weight gain."
"Male, wild-type CD-1 mice were divided into one of three groups (20 per group): high-fat (HF), HF + seed oil (HF + POMo) or lean control (LN). In HF and HF + POMo, mice were provided access ad libitum to a high-fat chow (60% of energy from fat). HF + POMo was supplemented with 61.79 mg POMo/d. LN consumed a restricted low-fat (10% of energy from fat) chow to maintain body weight within 5% of initial weight. Plasma was analysed for biomarkers associated with cholesterol profile (total cholesterol, HDL and TAG), glucose sensitivity (glucose and insulin), adipose tissue accumulation (leptin and adiponectin) and systemic low-grade inflammation (C-reactive protein and haptoglobin). The key findings of this study were that weight gain was associated with an increase in biomarkers of cholesterol profile, glucose sensitivity, adipose tissue accumulation and systemic low-grade inflammation (P <0.05). POMo only altered body weight accumulation, final body weight, leptin, adiponectin and insulin (P <0.05). We found that despite a similar level of energy intake, HF mice had a greater concentration of leptin and a lower concentration of adiponectin compared to HF + POMo mice," wrote B.K. Mcfarlin and colleagues, University of Houston.
The researchers concluded, "POMo intake was associated with an improvement in insulin sensitivity, suggesting that risk of developing type 2 diabetes may have been reduced; however, CVD risk did not change."
Mcfarlin and colleagues published their study in British Journal of Nutrition ("Pomegranate Seed Oil Consumption During a Period of High-fat Feeding Reduces Weight Gain and Reduces Type 2 Diabetes Risk in CD-1 Mice." British Journal of Nutrition, 2009;102(1):54-59).
For additional information, contact B.K. Mcfarlin, University of Houston, Dept. of Health & Human Performance, Laboratory Integrated Physiol, 3855 Holman St., 104U Garrison, Houston, TX 77204.
From the August 31, 2009, Prepared Foods E-dition