***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: The nutritional effects of butyrate on the colonic mucosa and studies of transformed cells suggest that butyrate has anti-colon cancer effects . If butyrate has antineoplastic effects , mucosal growth contrasts between normal subjects and those with a history of colonic neoplasia would parallel changes in growth characteristics caused by butyrate in a colon neoplasia population . To test this hypothesis , rectal biopsies from a survey of colonoscopy patients ( n = 50 ) with and without a history of colonic neoplasia ( controls ) were compared . Similarly , rectal biopsies were compared from subjects ( n = 44 ) with a colon neoplasia history in an acarbose-placebo crossover trial . Control subjects in the colonoscopy survey had higher bromodeoxyuridine ( BrdU ) uptake than subjects with a history of neoplasia ( P = 0.05 ) . The control subjects also had a higher correlation of BrdU and Ki-67 labeling ( P = 0.003 ) . Both findings were paralleled by acarbose use . Acarbose augmented BrdU uptake ( P = 0.0001 ) and improved the correlation of BrdU and Ki-67 labeling ( P = 0.013 ) . Acarbose also augmented fecal butyrate ( P = 0.0001 ) , which was positively correlated with Ki-67 labeling ( P = 0.003 ) . p52 antigen had an earlier pattern of crypt distribution in subjects with a history of colon neoplasia but was not affected by acarbose use . Lewis-Y antigen was expressed earlier in the crypt with acarbose but had similar expression in the colonoscopy survey groups . The use of acarbose to enhance fecal butyrate concentration produced mucosal changes paralleling the findings in control subjects as opposed to those with neoplasia , supporting the concept of an antineoplastic role for butyrate BACKGROUND The effects of acarbose add-on therapy on gut microbiota and inflammatory cytokines were investigated in Chinese patients with type 2 diabetes mellitus ( DM ) . METHODS Ninety-five DM patients were r and omly allocated to two groups : 59 to Group A who received antidiabetic treatment that included acarbose 150 mg/day  , and 36 to Group B who received similar treatment to Group A but without acarbose .  Forty-five healthy volunteers were selected as a control group . Serum concentrations of inflammatory cytokines were determined by ELISA , and the contents of 16S rDNA of gut bacteria were determined by real-time quantitative polymerase chain reaction . General linear analysis for repeated measurements was used to analyze trend differences between the two diabetic groups . RESULTS After 4 weeks of antidiabetic treatment , the gut contents of Bifidobacterium longum and Enterococcus faecalis were significantly increased in both diabetes groups . The increase of Bifidobacterium longum ( P = 0.004 ) and the decrease of lipopolysaccharides ( LPS ) ( P < 0.001 ) and prothrombin activator inhibitor-1 ( P = 0.003 ) were more significant in Group A. Decreases of monocyte chemoattractant protein-1 and LPS were more significant in patients whose HbA1c decrease was ≥1 % , but there were no significant differences in the changes of other cytokines and gut bacteria between patients with HbA1c < 7 % and ≥7 % . Pearson correlation analysis showed that changes of Enterococcus faecalis were negatively correlated with LPS , while multiple linear regression analysis showed a positive correlation of Bifidobacterium longum with acarbose treatment and the high-density lipoprotein cholesterol concentration . CONCLUSIONS Acarbose treatment can increase the content of gut Bifidobacterium longum in type 2 diabetes mellitus patients and decrease some inflammatory cytokines independently of its antihyperglycemic effects Aims /hypothesis Studies on the link between diabetes and bladder cancer in Asians are rare . We investigated the association between diabetes and incidence of bladder cancer by using a large national insurance data base . Methods A r and om sample of 1,000,000 individuals covered by the National Health Insurance was recruited . A total of 495,199 men and 503,748 women for all ages and 187,609 men and 189,762 women ≥40 years old and without bladder cancer at recruitment were followed from 2003 to 2005 . Cox regression evaluated the adjusted relative risk for all ages and for age ≥40 years old . Results The results were similar for all ages and for age ≥40 years . In Cox models , patients with diabetes consistently showed a significantly higher relative risk ranging from 1.36 to 1.51 after adjustment for age , sex and other potential confounders . Age , male sex , nephropathy , urinary tract diseases ( infection and stone ) and statin use were associated with bladder cancer , but occupation , hypertension , stroke , ischaemic heart disease , peripheral arterial disease , eye disease , dyslipidaemia and medications ( oral glucose-lowering agents including sulfonylurea , metformin , acarbose and thiazolidinediones , insulin , fibrates , ACE inhibitors/angiotensin receptor blockers and calcium channel blockers ) were not . Chronic obstructive pulmonary disease and living in regions other than Metropolitan Taipei were associated with lower risk . Conclusions Patients with diabetes have a higher risk of bladder cancer . The association with urinary tract diseases suggests a complex scenario in the link between bladder cancer and diabetes at different disease stages Flaws in the design , conduct , analysis , and reporting of r and omised trials can cause the effect of an intervention to be underestimated or overestimated . The Cochrane Collaboration ’s tool for assessing risk of bias aims to make the process clearer and more OBJECTIVE The link between diabetes and prostate cancer is rarely studied in Asians . RESEARCH DESIGN AND METHODS The trend of age-st and ardized prostate cancer incidence in 1995–2006 in the Taiwanese general population was calculated . A r and om sample of 1,000,000 subjects covered by the National Health Insurance in 2005 was recruited . A total of 494,630 men for all ages and 204,741 men ≥40 years old and without prostate cancer at the beginning of 2003 were followed to the end of 2005 .  Cumulative incidence and risk ratio between diabetic and nondiabetic men were calculated . Logistic regression estimated the adjusted odds ratios for risk factors . RESULTS The trend of prostate cancer incidence increased significantly ( P < 0.0001 ) . The cumulative incidence markedly increased with age in either the diabetic or nondiabetic men . The respective risk ratio ( 95 % CI ) for all ages and age 40–64 , 65–74 , and ≥75 years was 5.83 ( 5.10–6.66 ) , 2.09 ( 1.60–2.74 ) , 1.35 ( 1.07–1.71 ) , and 1.39 ( 1.12–1.71 ) . In logistic regression for all ages or for age ≥40 years , age , diabetes , nephropathy , ischemic heart disease , dyslipidemia , living region , and occupation were significantly associated with increased risk , but medications including insulin and oral antidiabetic agents were not . CONCLUSIONS Prostate cancer incidence is increasing in Taiwan . A positive link between diabetes and prostate cancer is observed , which is more remarkable in the youngest age of 40–64 years . The association between prostate cancer and comorbidities commonly seen in diabetic patients suggests a more complicated scenario in the link between prostate cancer and diabetes at different disease stages We investigated how fasting or postpr and ial insulin levels were altered by treatment with acarbose or sulfonylureas .  Plasma glucose and serum insulin , C-peptide , and proinsulin levels were measured before as well as 1 and 2 h after breakfast in 23 patients with non-insulin-dependent diabetes mellitus and 17 patients with impaired glucose tolerance . In the diabetic patients , 12 weeks of acarbose therapy decreased the postpr and ial levels of glucose ( 1 h : -60.0 % ; 2 h : -67.6 % ) , insulin ( 1 h : -67.5 % ; 2 h : -72.2 % ) and proinsulin ( 1 h : -55.2 % ; 2 h : -46.7 % ) , and proinsulin ( 1 h : -20.9 % ; 2 h : -57.5 % ) . In contrast , sulfonylurea treatment increased postpr and ial insulin and proinsulin levels . Since increased in the serum insulin or proinsulin levels are associated with a higher risk of cardiovascular disease , the present findings suggest that the acarbose-induced reduction of the postpr and ial serum insulin or proinsulin responses to food intake might be useful for preventing vascular complications in patients with diabetes AIMS To evaluate the efficacy and safety of linagliptin 5 and 10 mg vs. placebo and voglibose in Japanese patients with type 2 diabetes mellitus ( T2DM ) . METHODS This study enrolled patients with inadequately controlled T2DM who were previously treated with one or two oral antidiabetics or were drug naÏve . After a 2 to 4-week washout and placebo run-in , 561 patients were r and omized ( 2 : 2 : 2 : 1 ) to double-blind treatment with linagliptin 5 or 10 mg qd , voglibose 0.2 mg tid or placebo . The primary endpoint was the change from baseline in haemoglobin A1c ( HbA1c ) with linagliptin vs. placebo after 12 weeks and vs. voglibose after 26 weeks . RESULTS Baseline characteristics were well balanced across treatment groups ( overall mean HbA1c was 8.01 % ) . The adjusted mean ( 95 % confidence interval ) treatment differences at week 12 were -0.87 % ( -1.04 , -0.70 ; p < 0.0001 ) and -0.88 % ( -1.05 , -0.71 ; p < 0.0001 ) for linagliptin 5 and 10 mg vs. placebo and at week 26 were -0.32 % ( -0.49 , -0.15 ; p = 0.0003 ) and -0.39 % ( -0.56 , -0.21 ; p < 0.0001 ) for linagliptin 5 and 10 mg vs. voglibose . At week 12 , mean HbA1c was 7.58 , 7.48 and 8.34 % in patients receiving linagliptin 5 mg , linagliptin 10 mg and placebo , respectively . At week 26 , mean HbA1c was 7.63 % with linagliptin 5 mg , 7.50 % with linagliptin 10 mg and 7.91 % with voglibose . Drug-related adverse event rates were comparable across treatment groups over 12 weeks ( 9.4 % linagliptin 5 mg , 8.8 % linagliptin 10 mg and 10.0 % placebo ) and 26 weeks ( 11.3 % linagliptin 5 mg , 10.6 % linagliptin 10 mg and 18.5 % voglibose ) . There were no documented cases of hypoglycaemia .  CONCLUSIONS Linagliptin showed superior glucose-lowering efficacy and comparable safety and tolerability to both placebo and voglibose in Japanese patients with T2DM The use of nonsteroidal anti‐inflammatory drugs has been suggested to have a chemopreventive effect against colon carcinoma , through the inhibition of cyclooxygenases 1 and 2 , in patients with familial adenomatous polyposis and in animal models . Acarbose , an alpha‐glycosidase inhibitor , may also be chemopreventive . In order to examine the effects of these drugs we employed APC gene knockout mice r and omized into 3 groups , one for treatment with piroxicam ( 0.05 % concentration in drinking water ) , one for acarbose ( 0.04 % concentration in food ) and another for the control . After 14 weeks of treatment , mice were killed for quantitation of gastric and intestinal adenomas . Tumor multiplicity in the whole gastrointestinal tract decreased from 33.89±13.07 tumors/mouse in the control group to 17.05±7 tumors/mouse in the piroxicam‐treated group ( P<0.001 ) . The decrease in the acarbose‐treated group ( 29.68±12.86 tumors/mouse ) was not significant ( P>0.05 ) . The number of tumors ≥3 mm in diameter was also quantified in all gastrointestinal segments . The number of such tumors in the piroxicam group was decreased to 0.56±1.2 tumors/mouse from the control value of 3.78±1.17 tumors/mouse ( P<0.001 ) , while in the acarbose‐treated group the number decreased to 2.36±1.7 tumors/mouse ( P<0.01 ) . Thus , 
    Output:
    
Meta- analysis of r and omized controlled trials did not reveal any significant association between AGIs and cancer risk .
Meta- analysis of observational studies indicated that AGIs may decrease the risk of cancer in individuals with diabetes