***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: D iabetes is one of the most costly and burdensome chronic diseases of our time and is a condition that is increasing in epidemic proportions in the U.S. and throughout the world ( 1 ) . The complications result ing from the disease are a significant cause of morbidity and mortality and are associated with the damage or failure of various organs such as the eyes , kidneys , and nerves . Individuals with type 2 diabetes are also at a significantly higher risk for coronary heart disease , peripheral vascular disease , and stroke , and they have a greater likelihood of having hypertension , dyslipidemia , and obesity ( 2–6 ) . There is also growing evidence that at glucose levels above normal but below the diabetes threshold diagnostic now referred to as pre-diabetes , there is a substantially increased risk of cardiovascular disease ( CVD ) and death ( 5,7–10 ) . In these individuals , CVD risk factors are also more prevalent ( 5–7,9,11–14 ) , which further increases the risk but is not sufficient to totally explain it . In contrast to the clear benefit of glucose lowering to prevent or retard the progression of microvascular complications associated with diabetes ( 15– 18,21 ) , it is less clear whether the high rate of CVD in people with impaired glucose homeostasis , i.e. , those with impaired fasting glucose ( IFG ) , impaired glucose tolerance ( IGT ) , or diabetes , is caused by elevated blood glucose levels or will respond to treatments that lower blood glucose . Epidemiological studies have shown a clear relationship ( 19,20 ) , whereas intervention trials in people with diabetes suggest , but have not demonstrated , a clear benefit of glycemic control ( 15,16,21,22 ) . Additionally , there are no studies that have investigated a benefit of glucose lowering on macrovascular disease in subjects with only pre-diabetes ( IFG or IGT ) but not diabetes . Although the treatment of diabetes has become increasingly sophisticated , with over a dozen pharmacological agents available to lower blood glucose , a multitude of ancillary supplies and equipment available , and a clear recognition by health care professionals and patients that diabetes is a serious disease , the normalization of blood glucose for any appreciable period of time is seldom achieved ( 23 ) . In addition , in well-controlled socalled “ intensively ” treated patients , serious complications still occur ( 15–18,21 ) , and the economic and personal burden of diabetes remains . Furthermore , microvascular disease is already present in many individuals with undiagnosed or newly diagnosed type 2 diabetes ( 11,24– 28 ) . Given these facts , it is not surprising that studies have been initiated in the last decade to determine the feasibility and benefit of various strategies to prevent or delay the onset of  type 2 diabetes .  Two early reports ( 29,30 ) suggested that changes in lifestyle can prevent diabetes , but weaknesses in study design limited their general relevance . Recently , however , four well- design ed r and omized controlled trials have been reported ( 31–35 ) . In the Finnish study ( 31 ) , 522 middleaged ( mean age 55 years ) obese ( mean BMI 31 kg/m ) subjects with IGT were r and omized to receive either brief diet and exercise counseling ( control group ) or intensive individualized instruction on weight reduction , food intake , and guidance on increasing physical activity ( intervention group ) . After an average follow-up of 3.2 years , there was a 58 % relative reduction in the incidence of diabetes in the intervention group compared with the control subjects . A strong correlation was also seen between the ability to stop the progression to diabetes and the degree to which subjects were able to achieve one or more of the following : lose weight ( goal of 5.0 % weight reduction ) , reduce fat intake ( goal of 30 % of calories ) , reduce saturated fat intake ( goal of 10 % of calories ) , increase fiber intake ( goal of 15 g/1,000 kcal ) , and exercise ( goal of 150 min/week ) . No untoward effects of the lifestyle interventions were observed . In the Diabetes Prevention Program ( DPP ) ( 32–34 ) , the 3,234 enrolled subjects were slightly younger ( mean age 51 years ) and more obese ( mean BMI 34 kg/m ) but had nearly identical glucose intolerance compared with subjects in the Finnish study . About 45 % of the participants were from minority groups ( e.g , AfricanAmerican , Hispanic ) , and 20 % were 60 years of age . Subjects were r and omized to one of three intervention groups , which included the intensive nutrition and exercise counseling ( “ lifestyle ” ) group or either of two masked medication treatment groups : the biguanide metformin group or the placebo group . The latter interventions were combined with st and ard diet and exercise recommendations . After an average follow-up of 2.8 years ( range 1.8–4.6 years ) , a 58 % relative reduction in the progression to diabetes was observed in the lifestyle group ( absolute incidence 4.8 % ) , and a 31 % relative reduction in the progression of diabetes was observed in the metformin group ( absolute incidence 7.8 % ) compared with control subjects ( absolute incidence 11.0 % ) . ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● ● BACKGROUND Polyunsaturated fatty acids ( PUFAs ) and monounsaturated fatty acids ( MUFAs ) have been shown to positively affect blood lipids ; however , their comparative effects on insulin sensitivity are unclear . OBJECTIVE Our objective was to investigate whether chronic intake of MUFAs or PUFAs improves insulin sensitivity in people with type 2 diabetes via stimulation of the endogenous gut hormone glucagon-like peptide 1 [ 7 - 36 ] amide ( GLP-1 ) . DESIGN Nine overweight people with type 2 diabetes received isoenergetic high-MUFA ( 20.3 + /- 3.5 % of total energy ) or high-PUFA ( 13.4 + /- 1 . 3 % ) diets for 24 d in a r and omized , double-blind crossover design . RESULTS Weight and glycemic control remained stable throughout the study . Despite a significant change in the plasma triacylglycerol linoleic-oleic acid ratio ( L : O ) with both diets ( MUFA : from 0.46 + /- 0.03 to 0.29 + /- 0.02 , P : < 0.005 ; PUFA : from 0.36 + /- 0.04 to 0.56 + /- 0.05 , P : < 0.05 ) and the phospholipid L : O ( 1.7 + /- 0.1 to 2.0 + /- 0.3 ; P : = 0.04 ) during consumption of the PUFA diet , this change was not associated with a change in insulin sensitivity , measured by the short-insulin-tolerance test . There was a significant reduction in the ratio of total to HDL cholesterol during consumption of the PUFA diet ( 5.2 + /- 0.4 compared with 4.7 + /- 0.3 ; P : = 0.005 ) but no change with the MUFA diet . There was no change in the fasting or postpr and ial incremental area under the curve in response to an identical st and ard test meal for glucose , insulin , triacylglycerol , nonesterified fatty acids , or GLP-1 . CONCLUSIONS Over the 3-wk intervention period , diet-induced change in the triacylglycerol or phospholipid L : O was not associated with either increased stimulation of GLP-1 or a change in insulin sensitivity in people with type 2 diabetes Aims /hypothesis . The aim of the Diabetes Prevention Study is to assess the efficacy of an intensive diet-exercise programme in preventing or delaying  Type II ( non-insulin-dependent ) diabetes mellitus in subjects with impaired glucose tolerance , to evaluate the effects of the intervention programme on cardiovascular risk factors and to assess the determinants for the progression to diabetes in persons with impaired glucose tolerance . Methods . A total of 523 overweight subjects with impaired glucose tolerance ascertained by two oral glucose tolerance tests were r and omised to either a control or intervention group . The control subjects received general information at the start of the trial about the lifestyle changes necessary to prevent diabetes and about annual follow-up visits . The intervention subjects had seven sessions with a nutritionist during the first year and a visit every 3 months thereafter aim ed at reducing weight , the intake of saturated fat and increasing the intake of dietary fibre . Intervention subjects were also guided individually to increase their physical activity .  Results . During the first year , weight loss in the first 212 study subjects was 4.7 ± 5.5 vs 0.9 ± 4.1 kg in the intervention and control group , respectively ( p < 0.001 ) . The plasma glucose concentrations ( fasting : 5.9 ± 0.7 vs 6.4 ± 0.8 mmol/l , p < 0.001 ; and 2-h 7.8 ± 1.8 vs 8.5 ± 2.3 mmol/l , p < 0.05 ) were significantly lower in the intervention group after the first year of intervention . Favourable changes were also found in blood pressure , serum lipids and anthropometric indices in the intervention group . Conclusion /interpretation . The interim results show the efficacy and feasibility of the lifestyle intervention programme . [ Diabetologia ( 1999 ) 42 : 793–801 Context Weight loss and exercise decrease the development of diabetes in people with impaired glucose tolerance , but the effectiveness of these interventions in people with normal glucose tolerance is unknown . Contribution Using data from a large r and omized , controlled trial of cardiovascular disease prevention in men , the investigators show that participants with normal glucose tolerance at baseline developed diabetes at similar rates whether they received the diet and exercise intervention or usual care . However , the intervention was associated with lower risk of diabetes among nonsmokers . Implication s While diet and exercise may reduce the development of diabetes in nonsmokers with normal glucose metabolism at baseline , this benefit was not apparent among smokers . The Editors Epidemiologic studies have identified several potentially modifiable risk factors for type 2 diabetes mellitus , including obesity , a diet in which a high proportion of calories comes from fat , and low levels of physical activity ( 1 - 7 ) . Authorities have advocated that trials should test promising hypotheses about the primary prevention of type 2 diabetes ( 1 ) . R and omized intervention studies have demonstrated that , among those who already have impaired glucose tolerance , interventions that promote weight loss and increased exercise can reduce the risk for incident diabetes ( 8 - 10 ) . However , interventions should occur before at-risk individuals develop impaired glucose tolerance . A 2-year r and omized trial of diet , exercise , or both in individuals with a parental history of diabetes showed a statistically imprecise lower risk for developing diabetes in the intervention group ( 11 ) . To test such a hypothesis in groups who do not necessarily have a parental history of diabetes would be expensive . Strategies proposed for the primary prevention of type 2 diabetes include  weight reduction , reduced dietary fat intake , and increased exercise  ( 2 , 4 , 7 ) . These interventions are similar to those developed for preventing coronary heart disease ; therefore , examination of type 2 diabetes incidence rates in coronary heart disease prevention trials can provide preliminary evidence on the potential of such interventions to reduce type 2 diabetes risk . The Multiple Risk Factor Intervention Trial ( MRFIT ) enrolled 12866 middle-aged men at high risk for coronary heart disease and delivered either special intervention or usual care  over 6 to 7 years . The research ers obtained fasting glucose values yearly , and participants self-reported their use of insulin or oral hypoglycemic agents . The glucose values and reports of diabetes medication use enable estimation of diabetes incidence during the trial . Previous reports from MRFIT have described risk factors for the development of diabetes in the usual care group ( 12 ) and the risk for death associated with incident diabetes in the combined special intervention and usual care groups ( 13 ) . In this paper , we compare the incidence of diabetes in the  intervention and control groups of the MRFIT , report on an unexpected subgroup finding related to baseline cigarette smoking status , and explore reasons for the different results among smokers and nonsmokers . Methods Procedures Detailed descriptions of the MRFIT have been published ( 14 - 17 ) . Briefly , between 1973 and 1976 , the MRFIT investigators screened 361662 men for eligibility at 22 U.S. clinical centers . Of this group , 12866 men age 35 to 57 years were r and omly assigned : 6428 men to the special intervention group and 6438 men to the usual 
    Output:
    
There are no high quality data on the efficacy of dietary intervention for the prevention of type 2 diabetes .
More well- design ed , long-term studies , providing well-reported , high- quality data are required before proper conclusions can be made into the best dietary advice for the prevention of diabetes mellitus in adults