human
***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: OBJECTIVE The objective of this study was to determine potential added value of novel risk factors in predicting the development of  type 2 diabetes  beyond that provided by st and ard clinical risk factors . RESEARCH DESIGN AND METHODS The Atherosclerosis Risk in Communities ( ARIC ) Study is a population -based prospect i ve cohort study in four U.S. communities . Novel risk factors were either measured in the full cohort or in a case-control sample nested within the cohort . We started with a basic prediction model , previously vali date d in ARIC , and evaluated 35 novel risk factors by adding them independently to the basic model . The area under the curve ( AUC ) , net reclassification index ( NRI ) , and integrated discrimination index ( IDI ) were calculated to determine if each of the novel risk factors improved risk prediction . RESULTS There were 1,457 incident cases of diabetes with a mean of > 7.6 years of follow-up among 12,277 participants at risk . None of the novel risk factors significantly improved the AUC . Forced expiratory volume in 1 s was the only novel risk factor that result ed in a significant NRI ( 0.54 % ; 95 % CI : 0.33–0.86 % ) . Adiponectin , leptin , γ-glutamyl transferase , ferritin , intercellular adhesion molecule 1 , complement C3 , white blood cell count , albumin , activated partial thromboplastin time , factor VIII , magnesium , hip circumference , heart rate , and a genetic risk score each significantly improved the IDI , but net changes were small . CONCLUSIONS Evaluation of a large panel of novel risk factors for type 2 diabetes indicated only small improvements in risk prediction , which are unlikely to meaningfully alter clinical risk reclassification or discrimination strategies OBJECTIVE Hypomagnesemia occurs in 25–38 % of patients with type 2 diabetes . Several studies have suggested an association between magnesium ( Mg ) depletion and insulin resistance and /or reduction of insulin secretion in these cases . Our purpose was to evaluate if Mg supplementation ( as magnesium oxide [ MgO ] ) would improve metabolic control in patients with type 2 diabetes . RESEARCH DESIGN AND METHODS We studied 128 patients with type 2 diabetes ( 32 men , 96 women , aged 30–69 years ) , treated by diet or diet plus oral antidiabetic drugs , in the Bahia Federal University Hospital , Brazil . Patients at risk for hypomagnesemia or with reduced renal function were excluded . This study was a clinical r and omized double-blind placebo-controlled trial . Patients received either placebo , 20.7 mmol MgO , or 41.4 mmol MgO daily(elementary Mg ) for 30 days . Mg concentrations were measured in plasma , in mononuclear cells , and in 24-h urine sample s. Fasting blood glucose , HbA1 , and fructosamine were used as parameters of metabolic control . RESULTS Of the patients , 47.7 % had low plasma Mg , and 31.1 % had low intramononuclear Mg levels . Intracellular Mg in patients with diabetes was significantly lower than in the normal population ( 62 blood donors ; 1.4 ± 0.6 vs. 1.7 ± 0.6 μg/mg of total proteins ) . No correlation was found between plasma and intracellular Mg concentrations ( r = −0.179 ; P = 0.15 ) or between Mg concentrations and glycemic control ( r = −0.165 ; P = 0.12 ) . Intracellular Mg levels were lower in patients with peripheral neuropathy than in those without ( 1.2 ± 0.5 vs. 1.5 ± 0.6 μg/mg ) . Similar findings were observed in patients with coronary disease ( 1.0 ± 0.5 vs. 1.5 ± 0.6 μg/mg ) . In the placebo and in the 20.7 mmol Mg groups , neither a change in plasma and intracellular levels nor an improvement in glycemic control were observed . Replacement with 41.4 mmol Mg tended to increase plasma , cellular , and urine Mg and caused a significant fall ( 4.1 ± 0.8 to 3.8 ± 0.7 mmol/1 ) in fructosamine ( normal , 1.87–2.87 mmol/1 ) . CONCLUSIONS Mg depletion is common in poorly controlled patients with type 2 diabetes , especially in those with neuropathy or coronary disease . More prolonged use of Mg in doses that are higher than usual is needed toestablish its routine or selective administration in patients with type 2 diabetes to improve control or prevent chronic complications Literature data on the bioavailability of various Mg forms provide scarce information on the best Mg salt to be used in animal and human supplementation . This study aim ed to investigate the bioavailability of different forms of Mg in rats using Mg stable isotopes . Eighty male Wistar rats aged 6 weeks were fed a semi-purified Mg-depleted diet for three weeks . The rats were then r and omised into ten groups and received , for two more weeks , the same diet repleted with Mg ( 550 mg Mg/kg ) as : oxide , chloride , sulphate , carbonate , acetate , pidolate , citrate , gluconate , lactate or aspartate . After 10 days of Mg-repleted diet , the rats received orally 1.8 mg of an enriched 26Mg . Faeces and urine were then collected for 4 consecutive days . Isotope ratios in faeces and urine were determined . The Mg absorption values obtained varied from 50 % to 67 % . Organic Mg salts were slightly more available than inorganic Mg salts . Mg gluconate exhibited the highest Mg bioavailability of the ten Mg salts studied . Urinary 26Mg excretion varied from 0.20 mg to 0.33 mg , and feeding with the organic pidolate , citrate , gluconate and aspartate salts result ed in higher urinary 26Mg excretion than with inorganic salts . Ultimately , 26Mg retention was higher in the rats receiving the organic salts such as gluconate , lactate and aspartate than in those receiving the inorganic salts . Taken together , these results indicate that 26Mg is sufficiently bioavailable from the ten different Mg salts studied in the present experiment , although Mg gluconate exhibited the highest bioavailability under these experimental conditions Oral magnesium ( Mg ) supplementation can improve insulin sensitivity and secretion in patients with Type 2 diabetes mellitus ( DM ) . We studied the effect of Mg supplementation on glycaemic control , blood pressure , and plasma lipids in insulin-requiring patients with Type 2 DM . Fifty moderately controlled patients were r and omized to 15 mmol Mg or placebo daily for 3 months . Plasma Mg , glucose , HbA1c , lipids , erythrocyte Mg , Mg and glucose concentrations in 24-h urine , and systolic and diastolic pressure were measured before and after 3 months treatment . Plasma Mg concentration was higher after supplementation than after placebo ( 0.82 + /- 0.07 vs 0.78 + /- 0.08 mmol l(-1 ) , p < 0.05 ) , as was Mg excretion ( 5.5 + /- 1.9 vs 3.7 + /- 1.4 mmol 24 h(-1 ) , p = 0.004 ) but erythrocyte Mg concentrations were similar . No significant differences were found in glycaemic control ( glucose : 10.7 + /- 3.8 vs 11.6 + /- 6.2 mmol l(-1 ) , p = 0.8 ; HbA1c : 8.9 + /- 1.6 vs 9.1 + /- 1.2 % , p = 0.8 ) , lipids or blood pressure . On-treatment analysis ( 34 patients : 18 on Mg , 16 on placebo ) yielded similar results . An increase in plasma Mg concentration irrespective of medication was associated with a tendency to a decrease in diastolic pressure ( increased plasma Mg vs no increase : -4.0 + /- 10.1 vs + 2.5 + /- 12.0 mmHg , p = 0.059 ) . Three months ' oral Mg supplementation of insulin-requiring patients with Type 2 DM increased plasma Mg concentration and urinary Mg excretion but had no effect on glycaemic control or plasma lipid concentrations To evaluate the efficacy and safety of oral magnesium supplementation , with magnesium chloride ( MgCl2 ) , in the treatment of newly diagnosed depression in the elderly with type 2 diabetes and hypomagnesemia . Twenty-three elderly patients with type 2 diabetes and hypomagnesemia were enrolled and r and omly allocated to receive either 50 mL of MgCl2 5 % solution equivalent to 450 mg of elemental magnesium or Imipramine 50 mg daily during 12 weeks . Widowhood or divorce in the last six months , alcoholism , degenerative illnesses of the nervous central system , recent diagnosis of diabetes , previous or current treatment with antidepressants , chronic diarrhea , use of diuretics , and reduced renal function were exclusion criteria . Hypomagnesemia was defined by serum magnesium levels < 1.8 mg/dL and depression by Yasavage and Brink score > or = 11 points . The primary trial end point was the improvement of depression symptoms . At baseline , there were no differences by age ( 69 + /- 5.9 and 66.4 + /- 6.1 years , p = 0.39 ) , duration of diabetes ( 11.8 + /- 7.9 and 8.6 + /- 5.7 years , p = 0.33 ) , serum magnesium levels ( 1.3 + /- 0.04 and 1.4 + /- 0.04 mg/dL , p = 0.09 ) , and Yasavage and Brink Score ( 17.9 + /- 3.9 and 16.1 + /- 4.5 point , p = 0.34 ) in the groups with MgCl2 and imipramine , respectively . At end of follow-up , there were no significant differences in the Yasavage and Brink score ( 11.4 + /- 3.8 and 10.9 + /- 4.3 , p = 0.27 ) between the groups in study ; whereas serum magnesium levels were significantly higher in the group with MgCl2 ( 2.1 + /- 0.08 mg/dL ) than in the subjects with imipramine ( 1.5 + /- 0.07 mg/dL ) , p < 0.0005 . In conclusion , MgCl2 is as effective in the treatment of depressed elderly type 2 diabetics with hypomagnesemia as imipramine 50 mg daily We demonstrated similar plasma concentrations and urinary losses but lower erythrocyte magnesium concentrations ( 2.18 + /- 0.04 vs 1.86 + /- 0.03 mmol/L , P less than 0.01 ) in twelve aged ( 77.8 + /- 2.1 y ) vs 25 young ( 36.1 + /- 0.4 y ) , nonobese subjects . Subsequently , aged subjects were enrolled in a double-blind , r and omized , crossover study in which placebo ( for 4 wk ) and chronic magnesium administration ( CMA ) ( 4.5 g/d for 4 wk ) were provided . At the end of each treatment period an intravenous glucose tolerance test ( 0.33 g/kg body wt ) and a euglycemic glucose clamp with simultaneous [D-3H]glucose infusion and indirect calorimetry were performed . CMA vs placebo significantly increased erythrocyte magnesium concentration and improved insulin response and action . Net increase in erythrocyte magnesium significantly and positively correlated with the decrease in erythrocyte membrane microviscosity and with the net increase in both insulin secretion and action . In aged patients , correction of a low erythrocyte magnesium concentration may allow an improvement of glucose h and ling BACKGROUND AND AIMS It has been suggested that magnesium deficiency is associated with the triggering of acute phase response , which may contribute to type 2 diabetes and cardiovascular disease risk . We undertook this study to determine whether oral magnesium supplementation modifies serum levels of high-sensitivity C-reactive protein ( hsCRP ) in apparently healthy subjects with prediabetes and hypomagnesemia . METHODS A total of 62 men and non-pregnant women aged 18 - 65 year , with new diagnosis of prediabetes ( glucose 5.6 < 7.0 mmol/L and /or post-load glucose ≥7.7 < 11.1 mmol/L ) and hypomagnesemia ( serum magnesium levels < 0.74 mmol/L ) were enrolled in a clinical double-blind placebo-controlled trial and r and omly allocated to receive either magnesium chloride ( 3 
    Output:
    
agent
During subgroup analysis , a more beneficial effect of magnesium supplementation was observed in diabetic subjects with hypomagnesaemia .
CONCLUSIONS Magnesium supplementation can produce a favourable effect on FPG , HDL , LDL , TG and SBP .
***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: OBJECTIVE The objective of this study was to determine potential added value of novel risk factors in predicting the development of  type 2 diabetes  beyond that provided by st and ard clinical risk factors . RESEARCH DESIGN AND METHODS The Atherosclerosis Risk in Communities ( ARIC ) Study is a population -based prospect i ve cohort study in four U.S. communities . Novel risk factors were either measured in the full cohort or in a case-control sample nested within the cohort . We started with a basic prediction model , previously vali date d in ARIC , and evaluated 35 novel risk factors by adding them independently to the basic model . The area under the curve ( AUC ) , net reclassification index ( NRI ) , and integrated discrimination index ( IDI ) were calculated to determine if each of the novel risk factors improved risk prediction . RESULTS There were 1,457 incident cases of diabetes with a mean of > 7.6 years of follow-up among 12,277 participants at risk . None of the novel risk factors significantly improved the AUC . Forced expiratory volume in 1 s was the only novel risk factor that result ed in a significant NRI ( 0.54 % ; 95 % CI : 0.33–0.86 % ) . Adiponectin , leptin , γ-glutamyl transferase , ferritin , intercellular adhesion molecule 1 , complement C3 , white blood cell count , albumin , activated partial thromboplastin time , factor VIII , magnesium , hip circumference , heart rate , and a genetic risk score each significantly improved the IDI , but net changes were small . CONCLUSIONS Evaluation of a large panel of novel risk factors for type 2 diabetes indicated only small improvements in risk prediction , which are unlikely to meaningfully alter clinical risk reclassification or discrimination strategies OBJECTIVE Hypomagnesemia occurs in 25–38 % of patients with type 2 diabetes . Several studies have suggested an association between magnesium ( Mg ) depletion and insulin resistance and /or reduction of insulin secretion in these cases . Our purpose was to evaluate if Mg supplementation ( as magnesium oxide [ MgO ] ) would improve metabolic control in patients with type 2 diabetes . RESEARCH DESIGN AND METHODS We studied 128 patients with type 2 diabetes ( 32 men , 96 women , aged 30–69 years ) , treated by diet or diet plus oral antidiabetic drugs , in the Bahia Federal University Hospital , Brazil . Patients at risk for hypomagnesemia or with reduced renal function were excluded . This study was a clinical r and omized double-blind placebo-controlled trial . Patients received either placebo , 20.7 mmol MgO , or 41.4 mmol MgO daily(elementary Mg ) for 30 days . Mg concentrations were measured in plasma , in mononuclear cells , and in 24-h urine sample s. Fasting blood glucose , HbA1 , and fructosamine were used as parameters of metabolic control . RESULTS Of the patients , 47.7 % had low plasma Mg , and 31.1 % had low intramononuclear Mg levels . Intracellular Mg in patients with diabetes was significantly lower than in the normal population ( 62 blood donors ; 1.4 ± 0.6 vs. 1.7 ± 0.6 μg/mg of total proteins ) . No correlation was found between plasma and intracellular Mg concentrations ( r = −0.179 ; P = 0.15 ) or between Mg concentrations and glycemic control ( r = −0.165 ; P = 0.12 ) . Intracellular Mg levels were lower in patients with peripheral neuropathy than in those without ( 1.2 ± 0.5 vs. 1.5 ± 0.6 μg/mg ) . Similar findings were observed in patients with coronary disease ( 1.0 ± 0.5 vs. 1.5 ± 0.6 μg/mg ) . In the placebo and in the 20.7 mmol Mg groups , neither a change in plasma and intracellular levels nor an improvement in glycemic control were observed . Replacement with 41.4 mmol Mg tended to increase plasma , cellular , and urine Mg and caused a significant fall ( 4.1 ± 0.8 to 3.8 ± 0.7 mmol/1 ) in fructosamine ( normal , 1.87–2.87 mmol/1 ) . CONCLUSIONS Mg depletion is common in poorly controlled patients with type 2 diabetes , especially in those with neuropathy or coronary disease . More prolonged use of Mg in doses that are higher than usual is needed toestablish its routine or selective administration in patients with type 2 diabetes to improve control or prevent chronic complications Literature data on the bioavailability of various Mg forms provide scarce information on the best Mg salt to be used in animal and human supplementation . This study aim ed to investigate the bioavailability of different forms of Mg in rats using Mg stable isotopes . Eighty male Wistar rats aged 6 weeks were fed a semi-purified Mg-depleted diet for three weeks . The rats were then r and omised into ten groups and received , for two more weeks , the same diet repleted with Mg ( 550 mg Mg/kg ) as : oxide , chloride , sulphate , carbonate , acetate , pidolate , citrate , gluconate , lactate or aspartate . After 10 days of Mg-repleted diet , the rats received orally 1.8 mg of an enriched 26Mg . Faeces and urine were then collected for 4 consecutive days . Isotope ratios in faeces and urine were determined . The Mg absorption values obtained varied from 50 % to 67 % . Organic Mg salts were slightly more available than inorganic Mg salts . Mg gluconate exhibited the highest Mg bioavailability of the ten Mg salts studied . Urinary 26Mg excretion varied from 0.20 mg to 0.33 mg , and feeding with the organic pidolate , citrate , gluconate and aspartate salts result ed in higher urinary 26Mg excretion than with inorganic salts . Ultimately , 26Mg retention was higher in the rats receiving the organic salts such as gluconate , lactate and aspartate than in those receiving the inorganic salts . Taken together , these results indicate that 26Mg is sufficiently bioavailable from the ten different Mg salts studied in the present experiment , although Mg gluconate exhibited the highest bioavailability under these experimental conditions Oral magnesium ( Mg ) supplementation can improve insulin sensitivity and secretion in patients with Type 2 diabetes mellitus ( DM ) . We studied the effect of Mg supplementation on glycaemic control , blood pressure , and plasma lipids in insulin-requiring patients with Type 2 DM . Fifty moderately controlled patients were r and omized to 15 mmol Mg or placebo daily for 3 months . Plasma Mg , glucose , HbA1c , lipids , erythrocyte Mg , Mg and glucose concentrations in 24-h urine , and systolic and diastolic pressure were measured before and after 3 months treatment . Plasma Mg concentration was higher after supplementation than after placebo ( 0.82 + /- 0.07 vs 0.78 + /- 0.08 mmol l(-1 ) , p < 0.05 ) , as was Mg excretion ( 5.5 + /- 1.9 vs 3.7 + /- 1.4 mmol 24 h(-1 ) , p = 0.004 ) but erythrocyte Mg concentrations were similar . No significant differences were found in glycaemic control ( glucose : 10.7 + /- 3.8 vs 11.6 + /- 6.2 mmol l(-1 ) , p = 0.8 ; HbA1c : 8.9 + /- 1.6 vs 9.1 + /- 1.2 % , p = 0.8 ) , lipids or blood pressure . On-treatment analysis ( 34 patients : 18 on Mg , 16 on placebo ) yielded similar results . An increase in plasma Mg concentration irrespective of medication was associated with a tendency to a decrease in diastolic pressure ( increased plasma Mg vs no increase : -4.0 + /- 10.1 vs + 2.5 + /- 12.0 mmHg , p = 0.059 ) . Three months ' oral Mg supplementation of insulin-requiring patients with Type 2 DM increased plasma Mg concentration and urinary Mg excretion but had no effect on glycaemic control or plasma lipid concentrations To evaluate the efficacy and safety of oral magnesium supplementation , with magnesium chloride ( MgCl2 ) , in the treatment of newly diagnosed depression in the elderly with type 2 diabetes and hypomagnesemia . Twenty-three elderly patients with type 2 diabetes and hypomagnesemia were enrolled and r and omly allocated to receive either 50 mL of MgCl2 5 % solution equivalent to 450 mg of elemental magnesium or Imipramine 50 mg daily during 12 weeks . Widowhood or divorce in the last six months , alcoholism , degenerative illnesses of the nervous central system , recent diagnosis of diabetes , previous or current treatment with antidepressants , chronic diarrhea , use of diuretics , and reduced renal function were exclusion criteria . Hypomagnesemia was defined by serum magnesium levels < 1.8 mg/dL and depression by Yasavage and Brink score > or = 11 points . The primary trial end point was the improvement of depression symptoms . At baseline , there were no differences by age ( 69 + /- 5.9 and 66.4 + /- 6.1 years , p = 0.39 ) , duration of diabetes ( 11.8 + /- 7.9 and 8.6 + /- 5.7 years , p = 0.33 ) , serum magnesium levels ( 1.3 + /- 0.04 and 1.4 + /- 0.04 mg/dL , p = 0.09 ) , and Yasavage and Brink Score ( 17.9 + /- 3.9 and 16.1 + /- 4.5 point , p = 0.34 ) in the groups with MgCl2 and imipramine , respectively . At end of follow-up , there were no significant differences in the Yasavage and Brink score ( 11.4 + /- 3.8 and 10.9 + /- 4.3 , p = 0.27 ) between the groups in study ; whereas serum magnesium levels were significantly higher in the group with MgCl2 ( 2.1 + /- 0.08 mg/dL ) than in the subjects with imipramine ( 1.5 + /- 0.07 mg/dL ) , p < 0.0005 . In conclusion , MgCl2 is as effective in the treatment of depressed elderly type 2 diabetics with hypomagnesemia as imipramine 50 mg daily We demonstrated similar plasma concentrations and urinary losses but lower erythrocyte magnesium concentrations ( 2.18 + /- 0.04 vs 1.86 + /- 0.03 mmol/L , P less than 0.01 ) in twelve aged ( 77.8 + /- 2.1 y ) vs 25 young ( 36.1 + /- 0.4 y ) , nonobese subjects . Subsequently , aged subjects were enrolled in a double-blind , r and omized , crossover study in which placebo ( for 4 wk ) and chronic magnesium administration ( CMA ) ( 4.5 g/d for 4 wk ) were provided . At the end of each treatment period an intravenous glucose tolerance test ( 0.33 g/kg body wt ) and a euglycemic glucose clamp with simultaneous [D-3H]glucose infusion and indirect calorimetry were performed . CMA vs placebo significantly increased erythrocyte magnesium concentration and improved insulin response and action . Net increase in erythrocyte magnesium significantly and positively correlated with the decrease in erythrocyte membrane microviscosity and with the net increase in both insulin secretion and action . In aged patients , correction of a low erythrocyte magnesium concentration may allow an improvement of glucose h and ling BACKGROUND AND AIMS It has been suggested that magnesium deficiency is associated with the triggering of acute phase response , which may contribute to type 2 diabetes and cardiovascular disease risk . We undertook this study to determine whether oral magnesium supplementation modifies serum levels of high-sensitivity C-reactive protein ( hsCRP ) in apparently healthy subjects with prediabetes and hypomagnesemia . METHODS A total of 62 men and non-pregnant women aged 18 - 65 year , with new diagnosis of prediabetes ( glucose 5.6 < 7.0 mmol/L and /or post-load glucose ≥7.7 < 11.1 mmol/L ) and hypomagnesemia ( serum magnesium levels < 0.74 mmol/L ) were enrolled in a clinical double-blind placebo-controlled trial and r and omly allocated to receive either magnesium chloride ( 3 
    Output:
    