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1.
Med Sci Monit ; 25: 9377-9391, 2019 Dec 09.
Article in English | MEDLINE | ID: mdl-31815927

ABSTRACT

BACKGROUND Intestinal dysbiosis, or dysbacteriosis, is an abnormal interaction between the intestinal microbiota and the host cells due to altered microbial diversity. This study aimed to investigate the metabolic effects and changes in the intestinal microbiota in newborn rats following exposure to increased levels of maternal androgens in a rat model of maternal polycystic ovary syndrome (PCOS). MATERIAL AND METHODS The administration of androgen developed the rat maternal PCOS model during pregnancy. Maternal rat ovarian follicles were counting and assessed by histology. The metabolic phenotype of newborn rats was evaluated and included an insulin tolerance test, a glucose tolerance test, and measurement of serum levels of triglyceride, insulin, cholesterol, adiponectin, and leptin. Expression of pro-inflammatory cytokines was detected using quantitative reverse transcription-polymerase chain reaction (qRT-PCR), serum levels were measured by enzyme-linked immunosorbent assay (ELISA), and proteins associated with adipose tissue remodeling and adipocyte differentiation were measured by Western blot. RESULTS Markers of systemic inflammation were significantly increased in the female offspring but not in the male offspring born to rat in the PCOS model. Following birth, newborn rats that received antibiotics showed an improved metabolic phenotype, with reduced serum lipid levels, insulin resistance, body weight, inflammation of adipose tissue, and serum levels of inflammatory cytokines compared with controls. Probiotics had no significant effects on these parameters in newborn rats. CONCLUSIONS In a rat model of maternal PCOS, exposure to androgens in utero resulted in dysbiosis of the intestinal microbiota and metabolic disorders of the newborn female rats.


Subject(s)
Androgens/adverse effects , Gastrointestinal Microbiome/drug effects , Metabolic Diseases/etiology , Polycystic Ovary Syndrome/physiopathology , Adipose Tissue/metabolism , Animals , Animals, Newborn/metabolism , Body Weight , China , Disease Models, Animal , Dysbiosis , Female , Glucose/metabolism , Glucose Tolerance Test , Insulin/metabolism , Insulin Resistance , Leptin/metabolism , Male , Obesity/complications , Ovarian Follicle , Polycystic Ovary Syndrome/metabolism , Pregnancy , Prenatal Exposure Delayed Effects , Rats , Rats, Sprague-Dawley
2.
J Obes ; 2014: 495084, 2014.
Article in English | MEDLINE | ID: mdl-24782922

ABSTRACT

OBJECTIVE: To develop automatic visceral fat volume calculation software for computed tomography (CT) volume data and to evaluate its feasibility. METHODS: A total of 24 sets of whole-body CT volume data and anthropometric measurements were obtained, with three sets for each of four BMI categories (under 20, 20 to 25, 25 to 30, and over 30) in both sexes. True visceral fat volumes were defined on the basis of manual segmentation of the whole-body CT volume data by an experienced radiologist. Software to automatically calculate visceral fat volumes was developed using a region segmentation technique based on morphological analysis with CT value threshold. Automatically calculated visceral fat volumes were evaluated in terms of the correlation coefficient with the true volumes and the error relative to the true volume. RESULTS: Automatic visceral fat volume calculation results of all 24 data sets were obtained successfully and the average calculation time was 252.7 seconds/case. The correlation coefficients between the true visceral fat volume and the automatically calculated visceral fat volume were over 0.999. CONCLUSIONS: The newly developed software is feasible for calculating visceral fat volumes in a reasonable time and was proved to have high accuracy.


Subject(s)
Adiposity , Algorithms , Body Mass Index , Intra-Abdominal Fat , Software , Tomography, X-Ray Computed/methods , Cone-Beam Computed Tomography , Female , Humans , Image Processing, Computer-Assisted , Imaging, Three-Dimensional , Male , Software/standards
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