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ARS Home » Pacific West Area » Albany, California » Western Regional Research Center » Healthy Processed Foods Research » Research » Publications at this Location » Publication #207248
Title: Dietary soluble cellulose regulates fat metabolism and prevents obesity and insulin resistance in fat fed hamsters

Author
item Hong, Yun Jeong
item TUROWSKI, MACIEJ - DOW CHEMICAL CO., MI
item LYNCH, STEPHANIE - DOW CHEMICAL CO., MI
item SHAO, QIMING - SCIOS, FREMONT, CA
item CHEN, MINXIA - XIAN MED. UNIV., CHINA
item HU, WEI-SHOU - UNIV. OF MINNESOTA, MN
item Yokoyama, Wallace - Wally

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 12/26/2006
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Male Syrian hamsters fed 35% fat calorie diets become insulin resistant within a few weeks. Compared to a low-fat diet, the glucose infusion rate decreases by about 50% under conditions of the hyperinsulinemic euglycemic clamp methods. Longer term fat feeding results in obesity, hypertension, abdominal fat gain, increased plasma lipids, increased liver fat and other symptoms common to dietary metabolic diseases. The replacement of 5-8% insoluble fiber by soluble cellulose prevents most or all of these pathologies in the fat fed hamster. This model demonstrates that neither the dietary fat level, saturated fat level or carbohydrates alone are responsible for obesity-related metabolic diseases. This study also shows that soluble celluloses increase fecal lipid excretion, not only cholesterol and bile acids, but triglycerides and other fatty acyl glycerides. RT-PCR analysis shows that the hepatic gene, CYP51, is expressed at higher levels in soluble cellulose fed animals to maintain the cholesterol pool depleted by excretion of bile acids and cholesterol. Stearoyl Co-A Desaturase, SCD, is expressed at lower levels in the soluble cellulose fed hamsters, suggesting either lower levels of fat absorption or a decreased rate of fat absorption. The latter supports the excretion of fatty acyl glycerides in the feces.