Cheese consumption prevents fat accumulation in the liver and improves serum lipid parameters in rats fed a high-fat diet

International audienceAbstractCheese consumption has been reported to reduce the risk of metabolic syndrome; however, the mechanisms by which cheese prevents these disorders are not fully understood. The purpose of this study was to examine the effects of cheese consumption on lipid accumulation in the liver as well as to evaluate various serum lipid parameters. Two groups (n = 7) of male Fischer-344 rats were fed the following high-fat diets for 9 weeks: AIN76-modified 20% fat diet containing casein and butter oil (control diet) or the 20% fat diet containing a freeze-dried cheese powder (cheese diet). Blood samples, liver tissue, and fecal specimens were collected and analyzed. Cheese consumption for 9 weeks reduced the accumulation of triglyceride and cholesterol in the liver (P = 0.016 and P < 0.001, respectively), as well as the serum non-high-density lipoprotein (non-HDL) cholesterol concentration (P = 0.013). In contrast, cheese consumption increased the serum HDL concentration with statistical tendency (P = 0.086). We also observed an increase in the serum adiponectin concentration at week 9 in rats fed the cheese diet (P = 0.029). Furthermore, cheese consumption also increased fat excretion in the feces (P < 0.001). Taken together, our results suggest that cheese mediates various beneficial effects for preventing the development of metabolic syndrome by suppressing the accumulation of fat in the liver

Disruption of FADS2 gene in mice impairs male reproduction and causes dermal and intestinal ulceration

Delta-6 desaturase (D6D) catalyzes the first step in the synthesis of highly unsaturated fatty acids (HUFA) such as arachidonic (AA), docosapentaenoic (DPAn-6), and docosahexaenoic (DHA) acids, as well as the last desaturation of DPAn-6 and DHA. We created D6D-null mice (−/−), which enabled us to study HUFA deficiency without depleting their precursors. In −/−, no in vivo AA synthesis was detected after administration of [U-13C]linoleic acid (LA), indicating absence of D6D isozyme. Unexpectedly, all of the −/− developed ulcerative dermatitis when fed a purified diet lacking D6D products but containing ample LA. The −/− also exhibited splenomegaly and ulceration in duodenum and ileocecal junction. Male −/− lacked normal spermatozoa with a severe impairment of spermiogenesis. Tissue HUFAs in −/− declined differentially: liver AA and DHA by 95%, and a smaller decrease in brain and testes. Dietary AA completely prevented dermatitis and intestinal ulcers in −/−. DPAn-6 was absent in −/− brain under AA supplementation, indicating absence of D6D isozyme for DPAn-6 synthesis from AA. This study demonstrated a distinct advantage of the D6D-null mice (−/−) to elucidate (1) AA function without complication of LA deprivation and (2) DHA function in the nervous system without AA depletion or DPAn-6 replacement seen in traditional models.—Stroud, C. K., T. Y. Nara, M. Roqueta-Rivera, E. C. Radlowski, P. Lawrence, Y. Zhang, B. H. Cho, M. Segre, R. A. Hess, J. T. Brenna, W. M. Haschek, and M. T. Nakamura. Disruption of FADS2 gene in mice impairs male reproduction and causes dermal and intestinal ulceration