Long-Term Follow-Up of Colonoscopy Quality Monitoring.

INTRODUCTION: High-quality colonoscopy is paramount for colorectal cancer prevention. Since 2009, endoscopists at our institution have received quarterly report cards summarizing individual colonoscopy quality indicators. We have previously shown that implementing this intervention was associated with short-term improvement in adenoma detection rate (ADR). However, the long-term effect of continued monitoring on colonoscopy quality is unclear. METHODS: We conducted a retrospective study of prospectively administered quarterly colonoscopy quality report cards at the Roudebush Veteran's Affairs Medical Center between April 1, 2012, and August 31, 2019. The anonymized reports included individual endoscopists' ADRs, cecal intubation rates, and withdrawal times. Analyses were performed to determine slopes over time for each quality metric by physician and assess for differences based on whether ADRs were calculated quarterly or yearly. RESULTS: Data from the report cards of 17 endoscopists who had performed 24,361 colonoscopies were included. The mean quarterly ADR (±SD) was 51.7% (±11.7%) and mean yearly ADR was 47.2% (±13.8%). There was a small increase in overall ADR based on quarterly and yearly measurements (slope + 0.6%, P = 0.02; and slope +2.7%, P < 0.001, respectively), but no significant change in individual ADRs, cecal intubation rates, or withdrawal times. Analysis of SD of ADRs showed no significant difference between yearly and quarterly measurements ( P = 0.064). Individual endoscopists' ADR SD differences between yearly and quarterly measurements ranged from -4.7% to +6.8%. DISCUSSION: Long-term colonoscopy quality monitoring paralleled stable improvements in overall ADR. For endoscopists with baseline high ADR, frequent monitoring and reporting of colonoscopy quality metrics may not be necessary.

Glial cell line-derived neurotrophic factor protects against high-fat diet-induced obesity.

Obesity is a growing epidemic with limited effective treatments. The neurotrophic factor glial cell line-derived neurotrophic factor (GDNF) was recently shown to enhance ß-cell mass and improve glucose control in rodents. Its role in obesity is, however, not well characterized. In this study, we investigated the ability of GDNF to protect against high-fat diet (HFD)-induced obesity. GDNF transgenic (Tg) mice that overexpress GDNF under the control of the glial fibrillary acidic protein promoter and wild-type (WT) littermates were maintained on a HFD or regular rodent diet for 11 wk, and weight gain, energy expenditure, and insulin sensitivity were monitored. Differentiated mouse brown adipocytes and 3T3-L1 white adipocytes were used to study the effects of GDNF in vitro. Tg mice resisted the HFD-induced weight gain, insulin resistance, dyslipidemia, hyperleptinemia, and hepatic steatosis seen in WT mice despite similar food intake and activity levels. They exhibited significantly (P<0.001) higher energy expenditure than WT mice and increased expression in skeletal muscle and brown adipose tissue of peroxisome proliferator activated receptor-α and ß1- and ß3-adrenergic receptor genes, which are associated with increased lipolysis and enhanced lipid ß-oxidation. In vitro, GDNF enhanced ß-adrenergic-mediated cAMP release in brown adipocytes and suppressed lipid accumulation in differentiated 3T3L-1 cells through a p38MAPK signaling pathway. Our studies demonstrate a novel role for GDNF in the regulation of high-fat diet-induced obesity through increased energy expenditure. They show that GDNF and its receptor agonists may be potential targets for the treatment or prevention of obesity.

Is adiponectin involved in the pathogenesis of nonalcoholic steatohepatitis? A preliminary human study.

BACKGROUND: Animal studies have suggested that adiponectin may play a role in the pathogenesis of alcoholic and nonalcoholic fatty liver disease. Studies are limited that evaluated the role of adiponectin in the pathogenesis of nonalcoholic steatohepatitis (NASH). METHODS: To further our understanding of the role of adiponectin in the pathogenesis of NASH, the following studies were conducted. Serum adiponectin was measured and correlated with anthropometric and nutritional variables in 21 patients with biopsy-proven NASH and 19 age-, gender-, body mass index-, and body fat-matched controls. The effect of a mixed meal on serum adiponectin levels in a subgroup of patients (n = 24) with NASH and controls was assessed. In a separate cohort, liver samples belonging to healthy (n = 11), steatotic (n = 12), and NASH (n = 12) patients were used to further explore the role of adiponectin by measuring the expression of adiponectin and adiponectin receptor (AdipoR2) mRNA. RESULTS: Patients with NASH had significantly lower levels of serum adiponectin than controls (4.9 +/- 2.7 vs. 7.3 +/- 3.5 microg/mL, P = 0.02). While no significant correlation existed between serum adiponectin and anthropometric or nutritional variables, it was independently associated with age, high density lipoprotein, and triglycerides. Mixed meal had no effect on serum adiponectin either in patients with NASH or in controls. There was no expression of adiponectin mRNA in any of liver samples studied. However, AdipoR2 mRNA expression was higher in NASH than in steatotic and normal liver tissue. CONCLUSION: These data show that adiponectin may have a role in the pathogenesis of human NASH and should be investigated further.