Proceedings of the 3 rd International Conference on Obesity and Chronic Diseases ( ICOCD-2018 )

Obesity has been an epidemic in the US and world for more than two decades. Obesity is associated with serious health conditions, including type 2 diabetes, cardiovascular disease, certain types of cancers, hyperlipidemia, and liver steatosis. The intestinal microbiota is composed of a diverse population of obligate and facultative anaerobic microorganisms, and these organisms carry out a broad range of metabolic activities. Obesity has been linked to changes in the intestinal microbiota, but the composition of the bacterial populations in lean and obese Zucker rats has not been carefully studied. The objective of this study was to determine the effects of obesity on the gut microbiota in this model. Lean and obese female Zucker rats (n = 16) were fed an AIN-93G diet for 8 weeks. Rats were weighed twice weekly, and fecal samples were collected at the beginning and end of the experiment. 16S rRNA gene sequencing was used to evaluate the composition of the fecal bacterial populations. At the outset of the study, the lean rats exhibited much lower ratios of the Firmicutes to Bacteroidetes phyla than the obese rats, but after 60 days, this ratio in the lean rats exceeded that of the obese. Obese rats also showed increased levels of the genus Akkermansia at day 60. PCoA plots of beta diversity showed clustering of the different test groups, indicating clear differences in intestinal microbiota populations associated with both the time point of the study and the lean or obese status. Since obesity is linked to the risk of development of different chronic diseases, this model would be valuable for investigation of the interrelationship of obesity and the intestinal microbiota on the development of several human obesity-related diseases. The benefit of using this obese model is that rats become obese in a short period of time which provides a better translation to obese humans. Obesity and Osteoporosis: Vitamin D and Magnesium as “Add-on” Players Edita Stokic Clinical Center of Vojvodina, Medical Faculty, University of Novi Sad, Novi Sad, Serbia Abstract Obesity and osteoporosis are two global health challenges with an increasing prevalence and a high impact on mortality and morbidity in the world today. Since 1975 global age-standardized BMI in men has increased from 21.7 kg/m2 to 24.2 kg/m2 in 2014, and in women from 22.1 kg/m2 to 24.4 kg/m2 in 2014. Based on WHO diagnostic criteria it is estimated that approximately 22 million women and 5.5 million men aged between 50-84 years have osteoporosis. Due to demographic change in population, the number of people with osteoporosis will rise from 27.5 million in 2010 to 33.9 million in 2025, corresponding to an increase of 23%. Accumulating evidence supports a complex relationship between obesity, adipose tissue, fat distribution and osteoporosis. Obesity adversely affects bone homeostasis by a range of mechanisms such as a modification of bone-regulating hormones and vitamin D levels, increased oxidative stress and inflammation, and altered bone cell metabolism. There is a fat mass-bone complex interaction which is directly influenced by adipose tissue dysfunction and other hormonal dysregulations. The role of J of Obesity and Chronic DiseasesObesity and osteoporosis are two global health challenges with an increasing prevalence and a high impact on mortality and morbidity in the world today. Since 1975 global age-standardized BMI in men has increased from 21.7 kg/m2 to 24.2 kg/m2 in 2014, and in women from 22.1 kg/m2 to 24.4 kg/m2 in 2014. Based on WHO diagnostic criteria it is estimated that approximately 22 million women and 5.5 million men aged between 50-84 years have osteoporosis. Due to demographic change in population, the number of people with osteoporosis will rise from 27.5 million in 2010 to 33.9 million in 2025, corresponding to an increase of 23%. Accumulating evidence supports a complex relationship between obesity, adipose tissue, fat distribution and osteoporosis. Obesity adversely affects bone homeostasis by a range of mechanisms such as a modification of bone-regulating hormones and vitamin D levels, increased oxidative stress and inflammation, and altered bone cell metabolism. There is a fat mass-bone complex interaction which is directly influenced by adipose tissue dysfunction and other hormonal dysregulations. The role of J of Obesity and Chronic Diseases