The Experts below are selected from a list of 129618 Experts worldwide ranked by ideXlab platform
Rebecca L Robker - One of the best experts on this subject based on the ideXlab platform.
-
High Fat Diet causes lipotoxicity responses in cumulus oocyte complexes and decreased fertilization rates
Endocrinology, 2010Co-Authors: Linda Lin Yan Wu, Kylie R Dunning, Michelle Lane, Darryl L Russell, Robert J. Norman, Xing Yang, Rebecca L RobkerAbstract:In obesity, accumulation of lipid in nonadipose tissues, or lipotoxicity, is associated with endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and ultimately apoptosis. We have previously shown that obese women have increased triglycerides in follicular fluid; thus, the present study examined whether High-Fat Diet–induced obesity causes lipotoxicity in granulosa cells and the cumulus–oocyte complex (COC). Oocytes of mice fed a High-Fat Diet had dramatically increased lipid content and reduced mitochondrial membrane potential compared to those of mice fed a control Diet. COCs from mice fed a High-Fat Diet had increased expression of ER stress marker genes ATF4 and GRP78. Apoptosis was increased in granulosa and cumulus cells of mice fed a High-Fat Diet. Mice fed a High-Fat Diet also exhibited increased anovulation and decreased in vivo fertilization rates. Thus, lipid accumulation, ER stress, mitochondrial dysfunction, and apoptosis are markedly increased in ovarian cells of mice fed a High-Fat...
-
High Fat Diet causes lipotoxicity responses in cumulus oocyte complexes and decreased fertilization rates
Endocrinology, 2010Co-Authors: Kylie R Dunning, Michelle Lane, Darryl L Russell, Robert J. Norman, Xing Yang, Rebecca L RobkerAbstract:In obesity, accumulation of lipid in nonadipose tissues, or lipotoxicity, is associated with endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and ultimately apoptosis. We have previously shown that obese women have increased triglycerides in follicular fluid; thus, the present study examined whether High-Fat Diet-induced obesity causes lipotoxicity in granulosa cells and the cumulus-oocyte complex (COC). Oocytes of mice fed a High-Fat Diet had dramatically increased lipid content and reduced mitochondrial membrane potential compared to those of mice fed a control Diet. COCs from mice fed a High-Fat Diet had increased expression of ER stress marker genes ATF4 and GRP78. Apoptosis was increased in granulosa and cumulus cells of mice fed a High-Fat Diet. Mice fed a High-Fat Diet also exhibited increased anovulation and decreased in vivo fertilization rates. Thus, lipid accumulation, ER stress, mitochondrial dysfunction, and apoptosis are markedly increased in ovarian cells of mice fed a High-Fat Diet. ER stress markers were also analyzed in granulosa cells and follicular fluid from women with varying body mass indices (BMI). ATF4 was increased in granulosa cells and [Ca(2+)] in follicular fluid from obese women compared to nonobese women. These results indicate that lipotoxicity may be occurring in ovarian cells of obese women and may contribute to the reduced pregnancy rates observed in response to obesity.
Xing Yang - One of the best experts on this subject based on the ideXlab platform.
-
High Fat Diet causes lipotoxicity responses in cumulus oocyte complexes and decreased fertilization rates
Endocrinology, 2010Co-Authors: Linda Lin Yan Wu, Kylie R Dunning, Michelle Lane, Darryl L Russell, Robert J. Norman, Xing Yang, Rebecca L RobkerAbstract:In obesity, accumulation of lipid in nonadipose tissues, or lipotoxicity, is associated with endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and ultimately apoptosis. We have previously shown that obese women have increased triglycerides in follicular fluid; thus, the present study examined whether High-Fat Diet–induced obesity causes lipotoxicity in granulosa cells and the cumulus–oocyte complex (COC). Oocytes of mice fed a High-Fat Diet had dramatically increased lipid content and reduced mitochondrial membrane potential compared to those of mice fed a control Diet. COCs from mice fed a High-Fat Diet had increased expression of ER stress marker genes ATF4 and GRP78. Apoptosis was increased in granulosa and cumulus cells of mice fed a High-Fat Diet. Mice fed a High-Fat Diet also exhibited increased anovulation and decreased in vivo fertilization rates. Thus, lipid accumulation, ER stress, mitochondrial dysfunction, and apoptosis are markedly increased in ovarian cells of mice fed a High-Fat...
-
High Fat Diet causes lipotoxicity responses in cumulus oocyte complexes and decreased fertilization rates
Endocrinology, 2010Co-Authors: Kylie R Dunning, Michelle Lane, Darryl L Russell, Robert J. Norman, Xing Yang, Rebecca L RobkerAbstract:In obesity, accumulation of lipid in nonadipose tissues, or lipotoxicity, is associated with endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and ultimately apoptosis. We have previously shown that obese women have increased triglycerides in follicular fluid; thus, the present study examined whether High-Fat Diet-induced obesity causes lipotoxicity in granulosa cells and the cumulus-oocyte complex (COC). Oocytes of mice fed a High-Fat Diet had dramatically increased lipid content and reduced mitochondrial membrane potential compared to those of mice fed a control Diet. COCs from mice fed a High-Fat Diet had increased expression of ER stress marker genes ATF4 and GRP78. Apoptosis was increased in granulosa and cumulus cells of mice fed a High-Fat Diet. Mice fed a High-Fat Diet also exhibited increased anovulation and decreased in vivo fertilization rates. Thus, lipid accumulation, ER stress, mitochondrial dysfunction, and apoptosis are markedly increased in ovarian cells of mice fed a High-Fat Diet. ER stress markers were also analyzed in granulosa cells and follicular fluid from women with varying body mass indices (BMI). ATF4 was increased in granulosa cells and [Ca(2+)] in follicular fluid from obese women compared to nonobese women. These results indicate that lipotoxicity may be occurring in ovarian cells of obese women and may contribute to the reduced pregnancy rates observed in response to obesity.
Mina Desai - One of the best experts on this subject based on the ideXlab platform.
-
maternal High Fat Diet programs rat offspring hypertension and activates the adipose renin angiotensin system
American Journal of Obstetrics and Gynecology, 2013Co-Authors: Cristiane Guberman, Juanita K Jellyman, Guang Han, Michael G Ross, Mina DesaiAbstract:Objective A maternal High-Fat Diet creates an increased risk of offspring obesity and systemic hypertension. Although the renal renin-angiotensin system (RAS) is known to regulate blood pressure, it is now recognized that the RAS is also activated in adipose tissue during obesity. We hypothesized that programmed offspring hypertension is associated with the activation of the adipose tissue RAS in the offspring of obese rat dams. Study Design At 3 weeks of age, female rats were weaned to a High-Fat Diet (60% k/cal; n = 6) or control Diet (10% k/cal; n = 6). At 11 weeks of age, these rats were mated and continued on their respective Diets during pregnancy. After birth, at 1 day of age, subcutaneous adipose tissue was collected; litter size was standardized, and pups were cross-fostered to either control or High-Fat Diet dams, which created 4 study groups. At 21 days of age, offspring were weaned to control or High-Fat Diet. At 6 months of age, body Fat and blood pressure were measured. Thereafter, subcutaneous and retroperitoneal adipose tissue was harvested from male offspring. Protein expression of adipose tissue RAS components were determined by Western blotting. Results The maternal High-Fat Diet induced early and persistent alterations in offspring adipose RAS components. These changes were dependent on the period of exposure to the maternal High-Fat Diet, were adipose tissue specific (subcutaneous and retroperitoneal), and were exacerbated by a postnatal High-Fat Diet. Maternal High-Fat Diet increased adiposity and blood pressure in offspring, regardless of the period of exposure. Conclusion These findings suggest that programmed adiposity and the activation of the adipose tissue RAS are associated with hypertension in offspring of obese dams.
Son G Nguyen - One of the best experts on this subject based on the ideXlab platform.
-
laminarin favorably modulates gut microbiota in mice fed a High Fat Diet
Food & Function, 2016Co-Authors: Son G Nguyen, Jungman Kim, Robin B Guevarra, Jihoon Lee, Eungpil Kim, Suil Kim, Tatsuya UnnoAbstract:We investigated the anti-obesity effects of the potential prebiotic, laminarin, on mice fed a High-Fat Diet. A metagenomics approach was applied to characterize the ecological and functional differences of gut microbiota among mice fed a normal Diet (CTL), a High-Fat Diet (HFD), and a laminarin-supplemented High-Fat Diet (HFL). The HFL mice showed a slower weight gain than the HFD mice during the laminarin-feeding period, but the rate of weight gain increased after the termination of laminarin supplementation. Gut microbial community analysis showed clear differences between the CTL and HFD mice, whereas the HFL mice were between the two. A Higher abundance of carbohydrate active enzymes was observed in the HFL mice compared to the HFD mice, with especially notable increases in glycoside hydrolase and polysaccharide lyases. A significant decrease in Firmicutes and an increase in the Bacteroidetes phylum, especially the genus Bacteroides, were observed during laminarin ingestion. Laminarin ingestion altered the gut microbiota at the species level, which was re-shifted after termination of laminarin ingestion. Therefore, supplementing laminarin could reduce the adverse effects of a High-Fat Diet by shifting the gut microbiota towards a Higher energy metabolism. Thus, laminarin could be used to develop anti-obesity functional foods. Our results also suggest that laminarin would need to be consumed regularly in order to prevent or manage obesity.
Kylie R Dunning - One of the best experts on this subject based on the ideXlab platform.
-
High Fat Diet causes lipotoxicity responses in cumulus oocyte complexes and decreased fertilization rates
Endocrinology, 2010Co-Authors: Linda Lin Yan Wu, Kylie R Dunning, Michelle Lane, Darryl L Russell, Robert J. Norman, Xing Yang, Rebecca L RobkerAbstract:In obesity, accumulation of lipid in nonadipose tissues, or lipotoxicity, is associated with endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and ultimately apoptosis. We have previously shown that obese women have increased triglycerides in follicular fluid; thus, the present study examined whether High-Fat Diet–induced obesity causes lipotoxicity in granulosa cells and the cumulus–oocyte complex (COC). Oocytes of mice fed a High-Fat Diet had dramatically increased lipid content and reduced mitochondrial membrane potential compared to those of mice fed a control Diet. COCs from mice fed a High-Fat Diet had increased expression of ER stress marker genes ATF4 and GRP78. Apoptosis was increased in granulosa and cumulus cells of mice fed a High-Fat Diet. Mice fed a High-Fat Diet also exhibited increased anovulation and decreased in vivo fertilization rates. Thus, lipid accumulation, ER stress, mitochondrial dysfunction, and apoptosis are markedly increased in ovarian cells of mice fed a High-Fat...
-
High Fat Diet causes lipotoxicity responses in cumulus oocyte complexes and decreased fertilization rates
Endocrinology, 2010Co-Authors: Kylie R Dunning, Michelle Lane, Darryl L Russell, Robert J. Norman, Xing Yang, Rebecca L RobkerAbstract:In obesity, accumulation of lipid in nonadipose tissues, or lipotoxicity, is associated with endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and ultimately apoptosis. We have previously shown that obese women have increased triglycerides in follicular fluid; thus, the present study examined whether High-Fat Diet-induced obesity causes lipotoxicity in granulosa cells and the cumulus-oocyte complex (COC). Oocytes of mice fed a High-Fat Diet had dramatically increased lipid content and reduced mitochondrial membrane potential compared to those of mice fed a control Diet. COCs from mice fed a High-Fat Diet had increased expression of ER stress marker genes ATF4 and GRP78. Apoptosis was increased in granulosa and cumulus cells of mice fed a High-Fat Diet. Mice fed a High-Fat Diet also exhibited increased anovulation and decreased in vivo fertilization rates. Thus, lipid accumulation, ER stress, mitochondrial dysfunction, and apoptosis are markedly increased in ovarian cells of mice fed a High-Fat Diet. ER stress markers were also analyzed in granulosa cells and follicular fluid from women with varying body mass indices (BMI). ATF4 was increased in granulosa cells and [Ca(2+)] in follicular fluid from obese women compared to nonobese women. These results indicate that lipotoxicity may be occurring in ovarian cells of obese women and may contribute to the reduced pregnancy rates observed in response to obesity.