***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: BACKGROUND Incretin hormones , such as glucagon-like peptide 1 ( GLP-1 ) and glucose-dependent insulinotropic polypeptide ( GIP ) , play an important role in meal-related insulin secretion . We previously demonstrated that glutamine is a potent stimulus of GLP-1 secretion in vitro . OBJECTIVE Our objective was to determine whether glutamine increases circulating GLP-1 and GIP concentrations in vivo and , if so , whether this is associated with an increase in plasma insulin . DESIGN We recruited 8 healthy normal-weight volunteers ( LEAN ) , 8 obese individuals with type 2 diabetes or impaired glucose tolerance ( OB-DIAB ) and 8 obese nondiabetic control subjects ( OB-CON ) .  Oral glucose ( 75 g ) , glutamine ( 30 g ) , and water were administered on 3 separate days in r and om order , and plasma concentrations of GLP-1 , GIP , insulin , glucagon , and glucose were measured over 120 min . RESULTS Oral glucose led to increases in circulating GLP-1 concentrations , which peaked at 30 min in LEAN ( 31.9 + /- 5.7 pmol/L ) and OB-CON ( 24.3 + /- 2.1 pmol/L ) subjects and at 45 min in OB-DIAB subjects ( 19.5 + /- 1.8 pmol/L ) . Circulating GLP-1 concentrations increased in all study groups after glutamine ingestion , with peak concentrations at 30 min of 22.5 + /- 3.4 , 17.9 + /- 1.1 , and 17.3 + /- 3.4 pmol/L in LEAN , OB-CON , and OB-DIAB subjects , respectively . Glutamine also increased plasma GIP concentrations but less effectively than glucose . Consistent with the increases in GLP-1 and GIP , glutamine significantly increased circulating plasma insulin concentrations . Glutamine stimulated glucagon secretion in all 3 study groups . CONCLUSION Glutamine effectively increases circulating GLP-1 , GIP , and insulin concentrations in vivo and may represent a novel therapeutic approach to stimulating insulin secretion in obesity and type 2 diabetes Gastric emptying of a  liquid glucose meal  was measured with scintigraphic techniques in nine recently diagnosed Type 2 diabetic patients and nine sex- and age-matched nondiabetic control subjects . Seven of the nine Type 2 diabetic patients were receiving oral hypoglycemic therapy which was discontinued the evening prior to the study . The other two diabetic patients were taking no medication . The average gastric half-emptying time was 33.6 min ( s.e.m . = 3.2 ) for the diabetic patients and 64.6 min ( s.e.m . = 4.2 ) for the nondiabetic controls ( p = 0.0005 ) . These measurements indicate rapid gastric emptying in Type 2 diabetic patients which may contribute to worsening of glucose control in these patients OBJECTIVE In patients with type 2 diabetes , but not type 1 diabetes , abnormal secretion of incretins in response to oral nutrients has been described . In healthy youths , we recently reported accentuated glucagon-like peptide 1 ( GLP-1 ) secretion in response to a diet soda sweetened with sucralose and acesulfame-K. In this study , we examined the effect of diet soda on gut hormones in youths with diabetes . RESEARCH DESIGN AND METHODS Subjects aged 12–25 years with type 1 diabetes ( n = 9 ) or type 2 diabetes ( n = 10 ) , or healthy control participants ( n = 25 ) drank 240 mL cola-flavored caffeine-free diet soda or carbonated water , followed by a 75-g glucose load , in a r and omized , cross-over design . Glucose , C-peptide , GLP-1 , glucose-dependent insulinotropic peptide ( GIP ) , and peptide Tyr-Tyr ( PYY ) were measured for 180 min . Glucose and GLP-1 have previously been reported for the healthy control subjects . RESULTS GLP-1 area under the curve ( AUC ) was 43 % higher after ingestion of diet soda versus carbonated water in individuals with type 1 diabetes ( P = 0.020 ) , similar to control subjects ( 34 % higher , P = 0.029 ) , but was unaffected by diet soda in patients with type 2 diabetes ( P = 0.92 ) . Glucose , C-peptide , GIP , and PYY AUC were not statistically different between the two conditions in any group . CONCLUSIONS Ingestion of diet soda before a glucose load augmented GLP-1 secretion in type 1 diabetic and control subjects but not type 2 diabetic subjects . GIP and PYY secretion were not affected by diet soda . The clinical significance of this increased GLP-1 secretion , and its absence in youths with type 2 diabetes , needs to be determined In type-2 diabetes , the overall incretin effect is reduced . The present investigation was design ed to compare insulinotropic actions of exogenous incretin hormones ( gastric inhibitory peptide [ GIP ] and glucagon-like peptide 1 [ GLP-1 ] [ 7 - 36 amide ] ) in nine type-2 diabetic patients ( fasting plasma glucose 7.8 mmol/liter ; hemoglobin A1c 6.3 + /- 0.6 % ) and in nine age- and weight-matched normal subjects .  Synthetic human GIP ( 0.8 and 2.4 pmol/kg.min over 1 h each ) , GLP-1 [ 7 - 36 amide ] ( 0.4 and 1.2 pmol/kg.min over 1 h each ) , and placebo were administered under hyperglycemic clamp conditions ( 8.75 mmol/liter ) in separate experiments . Plasma GIP and GLP-1 [ 7 - 36 amide ] concentrations ( radioimmunoassay ) were comparable to those after oral glucose with the low , and clearly supraphysiological with the high infusion rates . Both GIP and GLP-1 [ 7 - 36 amide ] dose-dependently augmented insulin secretion ( insulin , C-peptide ) in both groups ( P < 0.05 ) . With GIP , the maximum effect in type-2 diabetic patients was significantly lower ( by 54 % ; P < 0.05 ) than in normal subjects . With GLP-1 [ 7 - 36 amide ] type-2 diabetic patients reached 71 % of the increments in C-peptide of normal subjects ( difference not significant ) . Glucagon was lowered during hyperglycemic clamps in normal subjects , but not in type-2 diabetic patients , and further by GLP-1 [ 7 - 36 amide ] in both groups ( P < 0.05 ) , but not by GIP . In conclusion , in mild type-2 diabetes , GLP-1 [ 7 - 36 amide ] , in contrast to GIP , retains much of its insulinotropic activity . It also lowers glucagon concentrations Exogenous glucagon-like peptide 1(GLP-1 ) bioactivity is preserved in type 2 diabetic patients , result ing the peptide administration in a near-normalization of plasma glucose mainly through its insulinotropic effect . GLP-1 also reduces meal-related insulin requirement in type 1 diabetic patients , suggesting an impairment of the entero-insular axis in both diabetic conditions . To investigate this metabolic dysfunction , we evaluated endogenous GLP-1 concentrations , both at fasting and in response to nutrient ingestion , in 16 type 1 diabetic patients ( age = 40.5 + /- 14yr , HbA1C = 7.8 + /- 1.5 % ) , 14 type 2 diabetics ( age = 56.5 + /- 13yr , HbA1C = 8.1 + /- 1.8 % ) , and 10 matched controls . In postabsorptive state , a mixed breakfast ( 230 KCal ) was administered to all subjects and blood sample s were collected for plasma glucose , insulin , C-peptide and GLP-1 determination during the following 3 hours . In normal subjects , the test meal induced a significant increase of GLP-1 ( 30 ' , 60 ' : p < 0.01 ) , returning the peptide values towards basal concentrations . In type 2 diabetic patients , fasting plasma GLP-1 was similar to controls ( 102.1 + /- 1.9 vs. 97.3 + /- 4.01 pg/ml ) , but nutrient ingestion failed to increase plasma peptide levels , which even decreased during the test ( p < 0.01 ) . Similarly , no increase in postpr and ial GLP-1 occurred in type 1 diabetics , in spite of maintained basal peptide secretion ( 106.5 + /- 1.5 pg/ml ) . With respect to controls , the test meal induced in both diabetic groups a significant increase in plasma glucagon levels at 60 ' ( p < 0.01 ) . In conclusion , either in condition of insulin resistance or insulin deficiency chronic hyperglycemia , which is a common feature of both metabolic disorders , could induce a progressive desensitization of intestinal L-cells with consequent peptide failure response to specific stimulation BACKGROUND Glucagon-like peptide 1 ( GLP-1 ) has been proposed as a treatment for type 2 diabetes . We have investigated the long-term effects of continuous administration of this peptide hormone in a 6-week pilot study . METHODS 20 patients with type 2 diabetes were alternately assigned continuous subcutaneous infusion of GLP-1 ( n=10 ) or saline ( n=10 ) for 6 weeks . Before ( week 0 ) and at weeks 1 and 6 , they underwent beta-cell function tests ( hyperglycaemic clamps ) , 8 h profiles of plasma glucose , insulin , C-peptide , glucagon , and free fatty acids , and appetite and side-effect ratings on 100 mm visual analogue scales ; at weeks 0 and 6 they also underwent dexascanning , measurement of insulin sensitivity ( hyperinsulinaemic euglycaemic clamps ) , haemoglobin A(1c ) , and fructosamine . The primary endpoints were haemoglobin A(1c ) concentration , 8-h profile of glucose concentration in plasma , and beta-cell function ( defined as the first-phase response to glucose and the maximum insulin secretory capacity of the cell ) . Analyses were per protocol . FINDINGS One patient assigned saline was excluded because no veins were accessible . In the remaining nine patients in that group , no significant changes were observed except an increase in fructosamine concentration ( p=0.0004 ) . In the GLP-1 group , fasting and 8 h mean plasma glucose decreased by 4.3 mmol/L and 5.5 mmol/L ( p<0.0001 ) . Haemoglobin A(1c ) decreased by 1.3 % ( p=0.003 ) and fructosamine fell to normal values ( p=0.0002 ) . Fasting and 8 h mean concentrations of free fatty acids decreased by 30 % and 23 % ( p=0.0005 and 0.01 , respectively ) . Gastric emptying was inhibited , bodyweight decreased by 1.9 kg , and appetite was reduced . Both insulin sensitivity and beta-cell function improved ( p=0.003 and p=0.003 , respectively ) . No important side-effects were seen . INTERPRETATION GLP-1 could be a new treatment for type 2 diabetes , though further investigation of the long-term effects of GLP-1 is needed Background Sleeve gastrectomy ( SG ) and Roux-en-Y gastric bypass ( RYGBP ) are associated with similar type 2 diabetes mellitus ( T2DM ) resolution rates for morbidly obese subjects . However , the mechanisms underlying the resolution of T2DM after SG have not been clarified to date . This study aim ed to compare the early changes in gastrointestinal hormones involved in insulin and glucagon secretion in morbidly obese T2DM subjects undergoing SG or RYGBP . Methods This prospect i ve study investigated 12 subjects with T2DM who had undergone SG ( n = 6 ) or RYGBP ( n = 6 ) . Five body mass index ( BMI ) -matched obese non-diabetic subjects and five BMI -matched obese diabetic subjects served as control subjects .  Glucose , insulin , glucagon , glucagon-like peptide 1 ( GLP-1 ) , glucose-dependent insulinotropic polypeptide ( GIP ) , and GLP-2 were determined after a st and ardized mixed liquid meal before surgery and 6 weeks afterward . Results After 6 weeks , five of the six subjects in each surgical group presented with T2DM remission , although the area under the curve (AUC)0–120 of glucose was greater than that of the non-diabetic control subjects ( P < 0.01 
    Output:
    
Fixed effects meta- analysis revealed higher peak plasma GLP-1 concentrations in patients with type 2 diabetes .
Meta-regression analyses showed that HbA1c and fasting plasma glucose predicted the outcomes iAUC and iAUC min−1 , respectively .
Conclusions /interpretationThe present analysis suggests that patients with type 2 diabetes , in general , do not exhibit reduced GLP-1 secretion in response to an OGTT or meal test , and that deteriorating glycaemic control may be associated with reduced GLP-1 secretion