A Laparoscopic Bipolar Cutting Forceps Can Assist In A Case Of Difficult Vaginal Hysterectomy
difficult; hysterectomy; limited; obese; Obstetrics & Gynecology; vagina
Fenton B W; Hutchings T; Flora R F; Fanning J
Journal of Minimally Invasive Gynecology
2006
2006-07
Journal Article or Conference Abstract Publication
<a href="http://doi.org/10.1016/j.jmig.2006.04.01" target="_blank" rel="noreferrer noopener">10.1016/j.jmig.2006.04.01</a>
Loss of FXR protects against diet-induced obesity and accelerates liver carcinogenesis in ob/ob mice.
Adipose Tissue; Adiposity/genetics; Animals; Brown/pathology; Carcinoma/etiology/*genetics; Cell Transformation; Cytoplasmic and Nuclear/*deficiency/genetics; Diet; Dietary Fats/metabolism; Energy Metabolism/genetics; Female; Gene Knockout Techniques; Glucose Intolerance/complications/genetics; High-Fat/*adverse effects; Intestinal Absorption; Knockout; Leptin/deficiency/genetics; Liver Neoplasms/etiology/*genetics; Liver/pathology; Male; Mice; Muscle; Neoplastic/genetics; Obese; Obesity/*etiology/genetics; Receptors; Sex Factors; Skeletal/metabolism; Weight Gain/genetics
Farnesoid X receptor (FXR) is known to play important regulatory roles in bile acid, lipid, and carbohydrate metabolism. Aged (\textgreater12 months old) Fxr(-/-) mice also develop spontaneous liver carcinomas. In this report, we used three mouse models to investigate the role of FXR deficiency in obesity. As compared with low-density lipoprotein receptor (Ldlr) knockout (Ldlr(-/-)) mice, the Ldlr(-/-)Fxr(-/-) double-knockout mice were highly resistant to diet-induced obesity, which was associated with increased expression of genes involved in energy metabolism in the skeletal muscle and brown adipose tissue. Such a striking effect of FXR deficiency on obesity on an Ldlr(-/-) background led us to investigate whether FXR deficiency alone is sufficient to affect obesity. As compared with wild-type mice, Fxr(-/-) mice showed resistance to diet-induced weight gain. Interestingly, only female Fxr(-/-) mice showed significant resistance to diet-induced obesity, which was accompanied by increased energy expenditure in these mice. Finally, we determined the effect of FXR deficiency on obesity in a genetically obese and diabetic mouse model. We generated ob(-/-)Fxr(-/-) mice that were deficient in both Leptin and Fxr. On a chow diet, ob(-/-)Fxr(-/-) mice gained less body weight and had reduced body fat mass as compared with ob/ob mice. In addition, we observed liver carcinomas in 43% of young (\textless11 months old) Ob(-/-)Fxr(-/-) mice. Together these data indicate that loss of FXR prevents diet-induced or genetic obesity and accelerates liver carcinogenesis under diabetic conditions.
Zhang Yanqiao; Ge Xuemei; Heemstra Lydia A; Chen Wei-Dong; Xu Jiesi; Smith Joseph L; Ma Huiyan; Kasim Neda; Edwards Peter A; Novak Colleen M
Molecular endocrinology (Baltimore, Md.)
2012
2012-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1210/me.2011-1157" target="_blank" rel="noreferrer noopener">10.1210/me.2011-1157</a>
The orphan nuclear receptor small heterodimer partner is required for thiazolidinedione effects in leptin-deficient mice.
Animals; Bile Acids and Salts/metabolism; Cytoplasmic and Nuclear/biosynthesis/*genetics/metabolism; Diabetes Mellitus/*drug therapy/genetics/metabolism; Gene Expression Regulation/drug effects; Glucose/metabolism; Hepatocytes/drug effects; Humans; Insulin Resistance/genetics; Insulin/*metabolism; Leptin/deficiency/genetics; Lipid Metabolism/drug effects; Messenger/genetics; Mice; Obese; PPAR gamma/*biosynthesis/genetics; Receptors; RNA; Thiazolidinediones/*administration & dosage
BACKGROUND: Small heterodimer partner (SHP, NR0B2) is involved in diverse metabolic pathways, including hepatic bile acid, lipid and glucose homeostasis, and has been implicated in effects on the peroxisome proliferator-activated receptor gamma (PPARgamma), a master regulator of adipogenesis and the receptor for antidiabetic drugs thiazolidinediones (TZDs). In this study, we aim to investigate the role of SHP in TZD response by comparing TZD-treated leptin-deficient (ob/ob) and leptin-, SHP-deficient (ob/ob;Shp(-/-)) double mutant mice. RESULTS: Both ob/ob and double mutant ob/ob;Shp(-/-) mice developed hyperglycemia, insulin resistance, and hyperlipidemia, but hepatic fat accumulation was decreased in the double mutant ob/ob;Shp(-/-) mice. PPARgamma2 mRNA levels were markedly lower in ob/ob;Shp(-/-) liver and decreased to a lesser extent in adipose tissue. The TZD troglitazone did not reduce glucose or circulating triglyceride levels in ob/ob;Shp(-/-) mice. Expression of the adipocytokines, such as adiponectin and resistin, was not stimulated by troglitazone treatment. Expression of hepatic lipogenic genes was also reduced in ob/ob;Shp(-/-) mice. Moreover, overexpression of SHP by adenovirus infection increased PPARgamma2 mRNA levels in mouse primary hepatocytes. CONCLUSIONS: Our results suggest that SHP is required for both antidiabetic and hypolipidemic effects of TZDs in ob/ob mice through regulation of PPARgamma expression.
Tseng Hsiu-Ting; Park Young Joo; Lee Yoon-Kwang; Moore David D
Journal of biomedical science
2015
2015-05
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1186/s12929-015-0133-3" target="_blank" rel="noreferrer noopener">10.1186/s12929-015-0133-3</a>