***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: We examined the in vivo metabolic effects of vanadyl sulfate ( VS ) in non-insulin-dependent diabetes mellitus ( NIDDM ) . Six NIDDM subjects treated with diet and /or sulfonylureas  were examined at the end of three consecutive periods : placebo for 2 wk , VS ( 100 mg/d ) for 3 wk , and placebo for 2 wk . Euglycemic hyperinsulinemic ( 30 mU/m2.min ) clamps and oral glucose tolerance tests were performed at the end of each study period . Glycemic control at baseline was poor ( fasting plasma glucose 210 + /- 19 mg/dl ; HbA1c 9.6 + /- 0.6 % ) and improved after treatment ( 181 + /- 14 mg/dl [ P < 0.05 ] , 8.8 + /- 0.6 % , [ P < 0.002 ] ) ; fasting and post-glucose tolerance test plasma insulin concentrations were unchanged . After VS , the glucose infusion rate during the clamp was increased ( by approximately 88 % , from 1.80 to 3.38 mg/kg.min , P < 0.0001 ) . This improvement was due to both enhanced insulin-mediated stimulation of glucose uptake ( rate of glucose disposal [ Rd ] , + 0.89 mg/kg.min ) and increased inhibition of HGP ( -0.74 mg/kg.min ) ( P < 0.0001 for both ) . Increased insulin-stimulated glycogen synthesis ( + 0.74 mg/kg.min , P < 0.0003 ) accounted for > 80 % of the increased Rd after VS , and the improvement in insulin sensitivity was maintained after the second placebo period . The Km of skeletal muscle glycogen synthase was lowered by approximately 30 % after VS treatment ( P < 0.05 ) . These results indicate that 3 wk of treatment with VS improves hepatic and peripheral insulin sensitivity in insulin-resistant NIDDM humans . These effects were sustained for up to 2 wk after discontinuation of VS We compared the effects of oral vanadyl sulfate ( 100 mg/day ) in moderately obese NIDDM and nondiabetic subjects .  Three-hour euglycemic-hyperinsulinemic ( insulin infusion 30 mU · m−2 · min−1 ) clamps were performed after 2 weeks of placebo and 3 weeks of vanadyl sulfate treatment in six nondiabetic control subjects ( age 37 ± 3 years ; BMI 29.5 ± 2.4 kg/m2 ) and seven NIDDM subjects ( age 53 ± 2 years ; BMI 28.7 ±1.8 kg/m2 ) . Glucose turnover ( [3 - 3H]glucose ) , glycolysis from plasma glucose , glycogen synthesis , and whole-body carbohydrate and lipid oxidation were evaluated . Decreases in fasting plasma glucose ( by ∼1.7 mmol/l ) and HbAlc ( both P < 0.05 ) were observed in NIDDM subjects during treatment ; plasma glucose was unchanged in control subjects . In the latter , the glucose infusion rate ( GIR ) required to maintain euglycemia ( 40.1 ± 5.7 and 38.1 ± 4.8 μmol · kg fat-free mass [FFM]−1 · min−1 ) and glucose disposal ( Rd ) ( 41.7 ± 5.7 and 38.9 ±4.7 μmol · kg FFM−1 · min−1 ) were similar during placebo and vanadyl sulfate administration , respectively . Hepatic glucose output ( HGO ) was completely suppressed in both studies . In contrast , in NIDDM subjects , vanadyl sulfate increased GIR ∼82 % ( 17.3 ± 4.7 to 30.9 ± 2.7 μmol · kg FFM−1 · min−1 , P < 0.05 ) ; this improvement in insulin sensitivity was due to both augmented stimulation of Rd ( 26.0 ±4.0 vs. 33.6 ± 2.22 μmol · kg FFM−1 · min−1 , P < 0.05 ) and enhanced suppression of HGO ( 7.7 ± 3.1 vs. 1.3 ± 0.9 μmol · kg FFM−1 · min−1 , P < 0.05 ) . Increased insulin-stimulated glycogen synthesis accounted for > 80 % of the increased Rd with vanadyl sulfate ( P < 0.005 ) , but plasma glucose flux via glycolysis was unchanged . In NIDDM  subjects , vanadyl sulfate was also associated with greater suppression of plasma free fatty acids ( FFAs ) ( P < 0.01 ) and lipid oxidation ( P < 0.05 ) during clamps . The reduction in HGO and increase in Rd were both highly correlated with the decline in plasma FFA concentrations during the clamp period ( P < 0.001 ) . In conclusion , small oral doses of vanadyl sulfate do not alter insulin sensitivity in nondiabetic subjects , but it does improve both hepatic and skeletal muscle insulin sensitivity in NIDDM subjects in part by enhancing insulin 's inhibitory effect on lipolysis . These data suggest that vanadyl sulfate may improve a defect in insulin signaling specific to NIDDM 
    Output:
    
Treatment with vanadium often results in gastrointestinal side-effects .
CONCLUSION There is no rigorous evidence that oral vanadium supplementation improves glycaemic control in type 2 diabetes .