To test the hypothesis that smoking cessation increases diabetes risk, possibly owing to cessation-related weight gain, Yeh and coworkers studied 10 892 middle-aged adults in the ARIC (Atherosclero... Background: Cigarette smoking is an established predictor of incident type 2 diabetes mellitus, but the effects of smoking cessation on diabetes risk are unknown. Objective: To test the hypothesis ...

OBJECTIVE: To examine trends in the prevalence of type 2 diabetes and related conditions in Asian Americans compared with non-Hispanic whites. RESEARCH DESIGN AND METHODS: We analyzed data from the National Health Interview Survey (NHIS) from 1997 to 2008 to construct a nationally representative sample of 230,503 U.S. adults aged ≥18 years. Of these adults, 11,056 identified themselves as Asian Americans and 219,447 as non-Hispanic whites. RESULTS: The age- and sex-adjusted prevalence of type 2 diabetes was higher in Asian Americans than in whites throughout the study period (4.3–8.2% vs. 3.8–6.0%), and there was a significant upward trend in both ethnic groups (P < 0.01). BMI also was increased in both groups, but age- and sex-adjusted BMI was consistently lower in Asian Americans. In fully adjusted logistic regression models, Asian Americans remained 30–50% more likely to have diabetes than their white counterparts. In addition, Asian Indians had the highest odds of prevalent type 2 diabetes, followed by Filipinos, other Asians, and Chinese. CONCLUSIONS: Compared with their white counterparts, Asian Americans have a significantly higher risk for type 2 diabetes, despite having substantially lower BMI. Additional investigation of this disparity is warranted, with the aim of tailoring optimal diabetes prevention strategies to Asian Americans.

OBJECTIVE: To determine the longer-term effects of metformin treatment and behavioral weight loss on gut microbiota and short-chain fatty acids (SCFAs).RESEARCH DESIGN AND METHODS: We conducted a 3-parallel-arm, randomized trial. We enrolled overweight/obese adults who had been treated for solid tumors but had no ongoing cancer treatment and randomized them (n = 121) to either 1) metformin (up to 2,000 mg), 2) coach-directed behavioral weight loss, or 3) self-directed care (control) for 12 months. We collected stool and serum at baseline (n = 114), 6 months (n = 109), and 12 months (n = 105). From stool, we extracted microbial DNA and conducted amplicon and metagenomic sequencing. We measured SCFAs and other biochemical parameters from fasting serum.RESULTS: Of the 121 participants, 79% were female and 46% were Black, and the mean age was 60 years. Only metformin treatment significantly altered microbiota composition. Compared with control, metformin treatment increased amplicon sequence variants for Escherichia (confirmed as Escherichia coli by metagenomic sequencing) and Ruminococcus torques and decreased Intestinibacter bartlettii at both 6 and 12 months and decreased the genus Roseburia, including R. faecis and R. intestinalis, at 12 months. Effects were similar in comparison of the metformin group with the behavioral weight loss group. Metformin versus control also increased butyrate, acetate, and valerate at 6 months (but not at 12 months). Behavioral weight loss versus control did not significantly alter microbiota composition but did increase acetate at 6 months (but not at 12 months). Increases in acetate were associated with decreases in fasting insulin. Additional whole-genome metagenomic sequencing of a subset of the metformin group showed that metformin altered 62 metagenomic functional pathways, including an acetate-producing pathway and three pathways in glucose metabolism.CONCLUSIONS: Metformin, but not behavioral weight loss, impacted gut microbiota composition at 6 months and 12 months. Both metformin and behavioral weight loss altered circulating SCFAs at 6 months, including increasing acetate, which correlated with lower fasting insulin. Future research is needed to elucidate whether the gut microboime mediates or modifies metformin’s health effects.

OBJECTIVE: Diabetes appears to increase risk for some cancers, but the association between preexisting diabetes and postoperative mortality in cancer patients is less clear. Our objective was to systematically review postoperative mortality in cancer patients with and without preexisting diabetes and summarize results using meta-analysis. RSEARCH DESIGN AND METHODS: We searched the Medical Literature Analysis and Retrieval System Online (MEDLINE) and Excerpta Medica Database (EMBASE) for articles published on or before 1 July 2009, including references of qualifying articles. We included English language investigations of short-term postoperative mortality after initial cancer treatment. Titles, abstracts, and articles were reviewed by at least two independent readers. Study population and design, results, and quality components were abstracted with standard protocols by one reviewer and checked for accuracy by additional reviewers. RESULTS: Of 8,828 titles identified in our original search, 20 articles met inclusion criteria for qualitative systematic review. Of these, 15 reported sufficient information to be combined in meta-analysis. Preexisting diabetes was associated with increased odds of postoperative mortality across all cancer types (OR = 1.85 [95% CI 1.40–2.45]). The risk associated with preexisting diabetes was attenuated but remained significant when we restricted the meta-analysis to models that controlled for confounders (1.51 [1.13–2.02]) or when we accounted for publication bias using the trim and fill method (1.52 [1.13–2.04]). CONCLUSIONS: Compared with their nondiabetic counterparts, cancer patients with preexisting diabetes are ∼50% more likely to die after surgery. Future research should investigate physiologic pathways to mortality risk and determine whether improvements in perioperative diabetes care can reduce postoperative mortality.

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