***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: Type 2 diabetes is a global public health crisis that threatens the economies of all nations , particularly developing countries . Fueled by rapid urbanization , nutrition transition , and increasingly sedentary lifestyles , the epidemic has grown in parallel with the worldwide rise in obesity . Asia 's large population and rapid economic development have made it an epicenter of the epidemic . Asian population s tend to develop diabetes at younger ages and lower BMI levels than Caucasians . Several factors contribute to accelerated diabetes epidemic in Asians , including the “ normal-weight metabolically obese ” phenotype ; high prevalence of smoking and heavy alcohol use ; high intake of refined carbohydrates ( e.g. , white rice ) ; and dramatically decreased physical activity levels . Poor nutrition in utero and in early life combined with overnutrition in later life may also play a role in Asia 's diabetes epidemic . Recent advances in genome-wide association studies have contributed substantially to our underst and ing of diabetes pathophysiology , but currently identified genetic loci are insufficient to explain ethnic differences in diabetes risk . Nonetheless , interactions between Westernized diet and lifestyle and genetic background may accelerate the growth of diabetes in the context of rapid nutrition transition . Epidemiologic studies and r and omized clinical trials show that type 2 diabetes is largely preventable through diet and lifestyle modifications . Translating these findings into practice , however , requires fundamental changes in public policies , the food and built environments , and health systems . To curb the escalating diabetes epidemic , primary prevention through promotion of a healthy diet and lifestyle should be a global public policy priority BACKGROUND The consumption of sucrose-sweetened soft drinks ( SSSDs ) has been associated with obesity , the metabolic syndrome , and cardiovascular disorders in observational and short-term intervention studies . Too few long-term intervention studies in humans have examined the effects of soft drinks . OBJECTIVE We compared the effects of SSSDs with those of isocaloric milk and a noncaloric soft drink on changes in total fat mass and ectopic fat deposition ( in liver and muscle tissue ) . DESIGN Overweight subjects ( n = 47 ) were r and omly assigned to 4 different test drinks ( 1 L/d for 6 mo ) : SSSD ( regular cola ) , isocaloric semiskim milk , aspartame-sweetened diet cola , and water . The amount of intrahepatic fat and intramyocellular fat was measured with (1)H-magnetic resonance spectroscopy . Other endpoints were fat mass , fat distribution ( dual-energy X-ray absorptiometry and magnetic resonance imaging ) , and metabolic risk factors . RESULTS The relative changes between baseline and the end of 6-mo intervention were significantly higher in the regular cola group than in the 3 other groups for liver fat ( 132 - 143 % , sex-adjusted mean ; P < 0.01 ) , skeletal muscle fat ( 117 - 221 % ; P < 0.05 ) , visceral fat ( 24 - 31 % ; P < 0.05 ) , blood triglycerides ( 32 % ; P < 0.01 ) , and total cholesterol ( 11 % ; P < 0.01 ) . Total fat mass was not significantly different between the 4 beverage groups . Milk and diet cola reduced systolic blood pressure by 10 - 15 % compared with regular cola ( P < 0.05 ) . Otherwise , diet cola had effects similar to those of water . CONCLUSION Daily intake of SSSDs for 6 mo increases ectopic fat accumulation and lipids compared with milk , diet cola , and water . Thus , daily intake of SSSDs is likely to enhance the risk of cardiovascular and metabolic diseases . This trial is registered at clinical trials.gov as NCT00777647 Twenty one healthy untrained male subjects were r and omized to follow a high-fat diet ( HFD ; 55 - 60E% fat , 25 - 30E% carbohydrate , and 15E% protein ) or a normal diet ( ND ; 25 - 35E% fat , 55 - 60E% carbohydrate , and 10 - 15E% protein ) for 2(1/2 ) wk . Diets were isocaloric and tailored individually to match energy expenditure . At 2(1/2 ) wk of diet , one 60-min bout of bicycle exercise ( 70 % of maximal oxygen uptake ) was performed . Muscle biopsies were obtained before and after the diet , immediately after exercise , and after 3-h recovery . Insulin sensitivity ( hyperinsulinemic-euglycemic clamp ) and intramyocellular triacylglycerol content did not change with the intervention in either group . Indexes of mitochondrial density were similar across the groups and intervention . Mitochondrial respiratory rates , measured in permeabilized muscle fibers , showed a 31 ± 11 and 26 ± 9 % exercise-induced increase ( P < 0.05 ) in state 3 ( glycolytic substrates ) and uncoupled respiration , respectively . However , in HFD this increase was abolished . At recovery , no change from resting respiration was seen in either group . With a lipid substrate ( octanoyl-carnitine with or without ADP ) , similar exercise-induced increases ( 31 - 62 % ) were seen in HFD and ND , but only in HFD was an elevated ( P < 0.05 ) respiratory rate seen at recovery . With HFD complex I and IV protein expression decreased ( P < 0.05 and P = 0.06 , respectively ) . A fat-rich diet induces marked changes in the mitochondrial electron transport system protein content and in exercise-induced mitochondrial substrate oxidation rates , with the effects being present hours after the exercise . The effect of HFD is present even without effects on insulin sensitivity and intramyocellular lipid accumulation . An isocaloric high-fat diet does not cause insulin resistance Consumption of simple carbohydrates has markedly increased over the past decades , and may be involved in the increased prevalence in metabolic diseases . Whether an increased intake of fructose is specifically related to a dysregulation of glucose and lipid metabolism remains controversial . We therefore compared the effects of hypercaloric diets enriched with fructose ( HFrD ) or glucose ( HGlcD ) in healthy men . Eleven subjects were studied in a r and omised order after 7 d of the following diets : ( 1 ) weight maintenance , control diet ; ( 2 ) HFrD ( 3.5 g fructose/kg fat-free mass ( ffm ) per d , + 35 % energy intake ) ; ( 3 ) HGlcD ( 3.5 g glucose/kg ffm per d , + 35 % energy intake ) . Fasting hepatic glucose output ( HGO ) was measured with 6,6 - 2H2-glucose . Intrahepatocellular lipids ( IHCL ) and intramyocellular lipids ( IMCL ) were measured by 1H magnetic resonance spectroscopy . Both fructose and glucose increased fasting VLDL-TAG ( HFrD : + 59 % , P < 0.05 ; HGlcD : + 31 % , P = 0.11 ) and IHCL ( HFrD : + 52 % , P < 0.05 ; HGlcD : + 58 % , P = 0.06 ) . HGO increased after both diets ( HFrD : + 5 % , P < 0.05 ; HGlcD : + 5 % , P = 0.05 ) . No change was observed in fasting glycaemia , insulin and alanine aminotransferase concentrations . IMCL increased significantly only after the HGlcD ( HFrD : + 24 % , NS ; HGlcD : + 59 % , P < 0.05 ) . IHCL and VLDL-TAG were not different between hypercaloric HFrD and HGlcD , but were increased compared to values observed with a weight maintenance diet . However , glucose led to a higher increase in IMCL than fructose It is currently believed that intramyocellular triglyceride ( IMTG ) accumulation and insulin resistance are a consequence of dietary fat ingestion and /or the elevated circulating lipid levels associated with chronic fat surplus . The purpose of this study was to compare the effect of short‐term starvation versus low‐carbohydrate (CHO)/high‐fat diet on IMTG accumulation and the development of insulin resistance in physically fit men . Intramyocellular triglyceride content , measured as intramyocellular lipid ( IMCL ) by proton magnetic resonance spectroscopy ( 1H‐MRS ) , and glucose tolerance/insulin sensitivity , assessed by frequently sample d intravenous glucose tolerance test ( IVGTT ) , were determined after 67 h of : ( a ) water‐only starvation ( S ) ; and ( b ) very low‐CHO/high‐fat diet ( LC ) . These diets had in common significant restriction of CHO availability but large differences in fat content . All results were compared with those measured after a mixed CHO diet ( C ) . Dietary interventions were administered by cross‐over design . The level of dietary‐induced IMTG accumulation ( P= 0.46 ) , insulin resistance ( P= 0.27 ) and glucose intolerance ( P= 0.29 ) was not different between S and LC treatments . Intramyocellular triglyceride content and insulin sensitivity were negatively correlated ( r=−0.63 , P < 0.01 ) . Therefore , whilst insulin resistance may be due to fat accumulation at a cellular level , in the integrated human organism this outcome is not exclusively a function of dietary fat intake . The comparable level of IMTG accumulation and insulin resistance following S and LC may suggest that these metabolic perturbations are largely a consequence of the increased lipolytic response associated with CHO restriction OBJECTIVE : To test the feasibility of creating a valid and reliable checklist with the following features : appropriate for assessing both r and omised and non-r and omised studies ; provision of both an overall score for study quality and a profile of scores not only for the quality of reporting , internal validity ( bias and confounding ) and power , but also for external validity . DESIGN : A pilot version was first developed , based on epidemiological principles , review s , and existing checklists for r and omised studies . Face and content validity were assessed by three experienced review ers and reliability was determined using two raters assessing 10 r and omised and 10 non-r and omised studies . Using different raters , the checklist was revised and tested for internal consistency ( Kuder-Richardson 20 ) , test-retest and inter-rater reliability ( Spearman correlation coefficient and sign rank test ; kappa statistics ) , criterion validity , and respondent burden . MAIN RESULTS : The performance of the checklist improved considerably after revision of a pilot version . The Quality Index had high internal consistency ( KR-20 : 0.89 ) as did the subscales apart from external validity ( KR-20 : 0.54 ) . Test-retest ( r 0.88 ) and inter-rater ( r 0.75 ) reliability of the Quality Index were good . Reliability of the subscales varied from good ( bias ) to poor ( external validity ) . The Quality Index correlated highly with an existing , established instrument for assessing r and omised studies ( r 0.90 ) . There was little difference between its performance with non-r and omised and with r and omised studies . Raters took about 20 minutes to assess each paper ( range 10 to 45 minutes ) . CONCLUSIONS : This study has shown that it is feasible to develop a checklist that can be used to assess the method ological quality not only of r and omised controlled trials but also non-r and omised studies . It has also shown that it is possible to produce a checklist that provides a profile of the paper , alerting review ers to its particular method ological strengths and weaknesses . Further work is required to improve the checklist and the training of raters in the assessment of external validity PURPOSE This study evaluated whether lowering IMCL stores via 3-d consumption of very-low-fat ( LFAT ) diet impairs endurance performance relative to a moderate-fat diet ( MFAT ) , and whether such a diet unfavorably alters lipid profiles . METHODS Twenty-one male and female endurance-trained runners followed a controlled diet and training regimen for 3 d prior to consuming either a LFAT ( 10 % fat ) or MFAT ( 35 % fat ) isoenergetic diet for another 3 d in r and om crossover fashion . On day 7 , runners followed a glycogen normalization protocol ( to equalize glycogen stores ) and then underwent performance testing ( 90-min preload run at 62 + /- 1 % VO2max followed by a 10-km time trial ) on the morning of day 8 . Muscle biopsies obtained from vastus lateralis before and after performance testing were analyzed for IMCL ( via electron microscopy ) and glycogen content ( via enzymatic methodology ) . RESULTS Despite approximately 30 % lower IMCL ( 0.220 + /- 0.032 % LFAT , 0.316 + /- 0.049 % MFAT ; P = 0.045 ) and approximately 22 % higher muscle glycogen stores at 
    Output:
    
Diets with an increased proportion of carbohydrates  decreased IMF proportions ; however , increasing caloric intake with carbohydrates increased IMF .
Starvation diets increased IMF stores , and hypocaloric diets did not result in any IMF proportion changes .
Conclusion This systematic review suggests that high-fat diets and diets with caloric intake increased above the amount required to maintain BMI with carbohydrates , and short-term starvation diets are associated with increases in IMF content .