Association of high dietary saturated fat intake and uncontrolled diabetes with constipation: evidence from the National Health and Nutrition Examination Survey.

BACKGROUND: Constipation is highly prevalent in the United States. The association of dietary fat intake with constipation has not been well studied. We recently reported that mice fed a high-fat diet had higher incidence of constipation than regular diet fed mice. The aim of this study was to assess if increased intake of dietary saturated fat in humans is also associated with higher risk of constipation and reduced stool frequency. METHODS: Analyses were based on data from 6207 adults (≥20 years) from the 2005-2006 and 2007-2008 cycles of the National Health and Nutrition Examination Surveys who had completed the bowel health questionnaire. Constipation was defined as a stool frequency of less than three times per week. Multivariable logistic regression analysis was used to calculate adjusted prevalence odds ratio (OR) estimates. Statistical analyses were performed using R and RStudio softwares. KEY RESULTS: The prevalence of constipation in this sample was 3.1%. After multivariable adjustment high saturated fat remained associated with constipation. The OR for high saturated fat intake associated with constipation was much higher in diabetics above 65 years, especially in non-Hispanic blacks, females, and those with poor glycemic control, compared to the control group. CONCLUSIONS & INFERENCES: To the best of our knowledge, this is the first report to investigate the association of high saturated fat diet, bowel frequency, and diabetes. This study demonstrates that a high dietary saturated fat intake is associated with significant increase in the prevalence of constipation, especially in the uncontrolled diabetic, non-Hispanic black, female patients.

Obesity and its associated disease: a role for microbiota?

BACKGROUND: Gut microbiota have recently been implicated in the pathogenesis of the obesity and its related metabolic diseases. A variety of factors including diet, genetic background, environment and host innate and adaptive immune responses define an individual's gut microbiota. PURPOSE: In this review we outline potential mechanisms by which gut microbiota can contribute to the development of obesity focusing on specific processes such as microbial energy extraction, microbiota induced-inflammation and regulation of appetite. We review the current understanding of each of these processes on regulating metabolism and examine potential therapeutic strategies for the treatment or prevention of the metabolic syndrome. We explore the hypothesis that alteration in gut microbiota may be an initial event leading to altered feeding behavior and/or systemic inflammation, ultimately leading to weight gain and the metabolic syndrome.

Role of the nitric oxide pathway and the endocannabinoid system in neurogenic relaxation of corpus cavernosum from biliary cirrhotic rats.

BACKGROUND AND PURPOSE: Relaxation of corpus cavernosum, which is mediated by nitric oxide (NO) released from non-adrenergic non-cholinergic (NANC) neurotransmission, is critical for inducing penile erection and can be affected by many pathophysiological conditions. However, the peripheral effect of liver cirrhosis on erectile function is as yet unknown. The aim of the present study was to investigate the effect of biliary cirrhosis on NANC-mediated relaxation of rat corpus cavernosum and the possible roles of endocannabinoid and nitric oxide systems in this model. EXPERIMENTAL APPROACH: Cirrhosis was induced by bile duct ligation. Controls underwent sham operation. Four weeks later, strips of corpus cavernosum were mounted in a standard organ bath and NANC-mediated relaxations were obtained by applying electrical field stimulation. KEY RESULTS: The NANC-mediated relaxation was enhanced in corporal strips from cirrhotic animals. Anandamide potentiated the relaxations in both groups. Either AM251 (CB(1) antagonist) or capsazepine (vanilloid VR(1) antagonist), but not AM630 (CB(2) antagonist), prevented the enhanced relaxations of cirrhotic strips. Either the non-selective NOS inhibitor L-NAME or the selective neuronal NOS inhibitor L-NPA inhibited relaxations in both groups, but cirrhotic groups were more resistant to the inhibitory effects of these agents. Relaxations to sodium nitroprusside (NO donor) were similar in tissues from the two groups. CONCLUSIONS AND IMPLICATIONS: Cirrhosis potentiates the neurogenic relaxation of rat corpus cavernosum probably via the NO pathway and involving cannabinoid CB(1) and vanilloid VR(1) receptors.