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Muhammad A Abdulghani - One of the best experts on this subject based on the ideXlab platform.
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empagliflozin treatment is associated with improved β cell function in type 2 diabetes mellitus
The Journal of Clinical Endocrinology and Metabolism, 2018Co-Authors: Hussein Al Jobori, Ralph A. Defronzo, Giuseppe Daniele, Eugenio Cersosimo, Curtis L Triplitt, John Adams, Carolina Solisherrera, Muhammad A AbdulghaniAbstract:Objective To examine whether lowering Plasma Glucose Concentration with the sodium-Glucose transporter-2 inhibitor empagliflozin improves β-cell function in patients with type 2 diabetes mellitus (T2DM). Methods Patients with T2DM (N = 15) received empagliflozin (25 mg/d) for 2 weeks. β-Cell function was measured with a nine-step hyperglycemic clamp (each step, 40 mg/dL) before and at 48 hours and at 14 days after initiating empagliflozin. Results Glucosuria was recorded on days 1 and 14 [mean ± standard error of the mean (SEM), 101 ± 10 g and 117 ± 11 g, respectively] after initiating empagliflozin, as were reductions in fasting Plasma Glucose levels (25 ± 6 mg/dL and 38 ± 8 mg/dL, respectively; both P < 0.05). After initiating empagliflozin and during the stepped hyperglycemic clamp, the incremental area under the Plasma C-peptide Concentration curve increased by 48% ± 12% at 48 hours and 61% ± 10% at 14 days (both P < 0.01); Glucose infusion rate increased by 15% on day 3 and 16% on day 14, compared with baseline (both P < 0.05); and β-cell function, measured with the insulin secretion/insulin resistance index, increased by 73% ± 21% at 48 hours and 112% ± 20% at 14 days (both P < 0.01). β-cell Glucose sensitivity during the hyperglycemic clamp was enhanced by 42% at 14 hours and 54% at 14 days after initiating empagliflozin (both P < 0.01). Conclusion Lowering the Plasma Glucose Concentration with empagliflozin in patients with T2DM augmented β-cell Glucose sensitivity and improved β-cell function.
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empagliflozin and kinetics of renal Glucose transport in healthy individuals and individuals with type 2 diabetes
Diabetes, 2017Co-Authors: Hussein Aljobori, Ralph A. Defronzo, Giuseppe Daniele, Eugenio Cersosimo, Curtis L Triplitt, Luke Norton, Rucha Mehta, Muhammad A AbdulghaniAbstract:Renal Glucose reabsorption was measured with the stepped hyperglycemic clamp in 15 subjects with type 2 diabetes mellitus (T2DM) and 15 without diabetes after 2 days and after more chronic (14 days) treatment with empagliflozin. Patients with T2DM had significantly greater maximal renal Glucose transport (TmG) compared with subjects without diabetes at baseline (459 ± 53 vs. 337 ± 25 mg/min; P < 0.05). Empagliflozin treatment for 48 h reduced the TmG in both individuals with and without diabetes by 44 ± 7 and 53 ± 6%, respectively (both P < 0.001). TmG was further reduced by empagliflozin in both groups on day 14 (by 65 ± 5 and 75 ± 3%, respectively). Empagliflozin reduced the Plasma Glucose Concentration threshold for Glucose spillage in the urine similarly in individuals with T2DM and without diabetes to <40 mg/dL, which is well below the normal fasting Plasma Glucose Concentration. In summary, sodium-Glucose transporter-2 inhibition with empagliflozin reduces both TmG and threshold for Glucose spillage in the urine in patients with T2DM and those without diabetes.
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prediabetes and risk of diabetes and associated complications impaired fasting Glucose versus impaired Glucose tolerance does it matter
Current Opinion in Clinical Nutrition and Metabolic Care, 2016Co-Authors: Muhammad A Abdulghani, Ralph A. Defronzo, Amin JayyousiAbstract:Purpose of review The purpose of this review is to summarize the distinct metabolic and pathophysiologic phenotype of impaired fasting Glucose (IFG) and impaired Glucose tolerance (IGT) and the subsequent clinical implications with regard to future type 2 diabetes mellitus (T2DM) and cardiovascular risk. Recent findings Both IFG and IGT manifest the two core defects of T2DM, that is, insulin resistance and β-cell dysfunction. However, the site of insulin resistance and shape of β-cell dysfunction differ. These distinct metabolic and pathophysiologic phenotypes explain the greater cardiovascular disease (CVD) risk associated with an increase in the 2-h Plasma Glucose Concentration, that is, IGT compared with an increase in the fasting Plasma Glucose (FPG) Concentration, that is, IFG. Moreover, the increase in future T2DM risk in IFG study participants is, at least in part, explained by the strong correlation between the increase in FPG and the increase in 2-h Plasma Glucose Concentration. Summary Last, recent studies have reported the presence of diabetic microvascular complications, that is, retinopathy and neuropathy, at the IGT stage.Thus, a Glucose load (e.g. oral Glucose tolerance test) is required in study participants with elevated FPG Concentration to accurately assess their future risk for T2DM, as well as their risk for CVD to identify the subgroup of IFG who are at greater risk and subject them to an intervention program to decrease their future T2DM and CVD risk.
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dapagliflozin lowers Plasma Glucose Concentration and improves β cell function
The Journal of Clinical Endocrinology and Metabolism, 2015Co-Authors: Aurora Merovci, Muhammad A Abdulghani, Giuseppe Daniele, Andrea Mari, Carolina Solis, Juan Xiong, Alberto Chavezvelazquez, Devjit Tripathy, Scheherezada Urban Mccarthy, Ralph A. DefronzoAbstract:Background: β-Cell dysfunction is a core defect in T2DM, and chronic, sustained hyperglycemia has been implicated in progressive β-cell failure, ie, glucotoxicity. The aim of the present study was to examine the effect of lowering the Plasma Glucose Concentration with dapagliflozin, a glucosuric agent, on β-cell function in T2DM individuals. Research Design and Methods: Twenty-four subjects with T2DM received dapagliflozin (n = 16) or placebo (n = 8) for 2 weeks, and a 75-g oral Glucose tolerance test (OGTT) and insulin clamp were performed before and after treatment. Plasma Glucose, insulin, and C-peptide Concentrations were measured during the OGTT. Results: Dapagliflozin significantly lowered both the fasting and 2-hour Plasma Glucose Concentrations and the incremental area under the Plasma Glucose Concentration curve (ΔG0–120) during OGTT by −33 ± 5 mg/dL, −73 ± 9 mg/dL, and −60 ± 12 mg/dL · min, respectively, compared to −13 ± 9, −33 ± 13, and −18 ± 9 reductions in placebo-treated subjects (both P < ...
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lowering Plasma Glucose Concentration by inhibiting renal sodium Glucose cotransport
Journal of Internal Medicine, 2014Co-Authors: Muhammad A Abdulghani, Ralph A. DefronzoAbstract:Maintaining normoglycaemia not only reduces the risk of diabetic microvascular complications but also corrects the metabolic abnormalities that contribute to the development and progression of hyperglycaemia, that is insulin resistance and beta-cell dysfunction. Progressive beta-cell failure, in addition to side effects associated with many current antidiabetic agents, for example hypoglycaemia and weight gain, presents major obstacles to the achievement of the recommended goal of glycaemic control in patients with type 2 diabetes mellitus (T2DM). Thus, novel effective therapies are needed for optimal Glucose control in subjects with T2DM. Most recently, specific inhibitors of the renal sodium–Glucose cotransporter 2 (SGLT2) have been developed to produce glucosuria and lower the Plasma Glucose Concentration. Because of the iR unique mechanism of action, which is independent of insulin secretion and insulin action, these agents are effective in lowering the Plasma Glucose Concentration in all stages of the disease and can be combined with all other antidiabetic agents. In this review, we will summarize the available data concerning the mechanism of action, efficacy and safety of this novel class of antidiabetic agents.
Ralph A. Defronzo - One of the best experts on this subject based on the ideXlab platform.
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empagliflozin treatment is associated with improved β cell function in type 2 diabetes mellitus
The Journal of Clinical Endocrinology and Metabolism, 2018Co-Authors: Hussein Al Jobori, Ralph A. Defronzo, Giuseppe Daniele, Eugenio Cersosimo, Curtis L Triplitt, John Adams, Carolina Solisherrera, Muhammad A AbdulghaniAbstract:Objective To examine whether lowering Plasma Glucose Concentration with the sodium-Glucose transporter-2 inhibitor empagliflozin improves β-cell function in patients with type 2 diabetes mellitus (T2DM). Methods Patients with T2DM (N = 15) received empagliflozin (25 mg/d) for 2 weeks. β-Cell function was measured with a nine-step hyperglycemic clamp (each step, 40 mg/dL) before and at 48 hours and at 14 days after initiating empagliflozin. Results Glucosuria was recorded on days 1 and 14 [mean ± standard error of the mean (SEM), 101 ± 10 g and 117 ± 11 g, respectively] after initiating empagliflozin, as were reductions in fasting Plasma Glucose levels (25 ± 6 mg/dL and 38 ± 8 mg/dL, respectively; both P < 0.05). After initiating empagliflozin and during the stepped hyperglycemic clamp, the incremental area under the Plasma C-peptide Concentration curve increased by 48% ± 12% at 48 hours and 61% ± 10% at 14 days (both P < 0.01); Glucose infusion rate increased by 15% on day 3 and 16% on day 14, compared with baseline (both P < 0.05); and β-cell function, measured with the insulin secretion/insulin resistance index, increased by 73% ± 21% at 48 hours and 112% ± 20% at 14 days (both P < 0.01). β-cell Glucose sensitivity during the hyperglycemic clamp was enhanced by 42% at 14 hours and 54% at 14 days after initiating empagliflozin (both P < 0.01). Conclusion Lowering the Plasma Glucose Concentration with empagliflozin in patients with T2DM augmented β-cell Glucose sensitivity and improved β-cell function.
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empagliflozin and kinetics of renal Glucose transport in healthy individuals and individuals with type 2 diabetes
Diabetes, 2017Co-Authors: Hussein Aljobori, Ralph A. Defronzo, Giuseppe Daniele, Eugenio Cersosimo, Curtis L Triplitt, Luke Norton, Rucha Mehta, Muhammad A AbdulghaniAbstract:Renal Glucose reabsorption was measured with the stepped hyperglycemic clamp in 15 subjects with type 2 diabetes mellitus (T2DM) and 15 without diabetes after 2 days and after more chronic (14 days) treatment with empagliflozin. Patients with T2DM had significantly greater maximal renal Glucose transport (TmG) compared with subjects without diabetes at baseline (459 ± 53 vs. 337 ± 25 mg/min; P < 0.05). Empagliflozin treatment for 48 h reduced the TmG in both individuals with and without diabetes by 44 ± 7 and 53 ± 6%, respectively (both P < 0.001). TmG was further reduced by empagliflozin in both groups on day 14 (by 65 ± 5 and 75 ± 3%, respectively). Empagliflozin reduced the Plasma Glucose Concentration threshold for Glucose spillage in the urine similarly in individuals with T2DM and without diabetes to <40 mg/dL, which is well below the normal fasting Plasma Glucose Concentration. In summary, sodium-Glucose transporter-2 inhibition with empagliflozin reduces both TmG and threshold for Glucose spillage in the urine in patients with T2DM and those without diabetes.
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prediabetes and risk of diabetes and associated complications impaired fasting Glucose versus impaired Glucose tolerance does it matter
Current Opinion in Clinical Nutrition and Metabolic Care, 2016Co-Authors: Muhammad A Abdulghani, Ralph A. Defronzo, Amin JayyousiAbstract:Purpose of review The purpose of this review is to summarize the distinct metabolic and pathophysiologic phenotype of impaired fasting Glucose (IFG) and impaired Glucose tolerance (IGT) and the subsequent clinical implications with regard to future type 2 diabetes mellitus (T2DM) and cardiovascular risk. Recent findings Both IFG and IGT manifest the two core defects of T2DM, that is, insulin resistance and β-cell dysfunction. However, the site of insulin resistance and shape of β-cell dysfunction differ. These distinct metabolic and pathophysiologic phenotypes explain the greater cardiovascular disease (CVD) risk associated with an increase in the 2-h Plasma Glucose Concentration, that is, IGT compared with an increase in the fasting Plasma Glucose (FPG) Concentration, that is, IFG. Moreover, the increase in future T2DM risk in IFG study participants is, at least in part, explained by the strong correlation between the increase in FPG and the increase in 2-h Plasma Glucose Concentration. Summary Last, recent studies have reported the presence of diabetic microvascular complications, that is, retinopathy and neuropathy, at the IGT stage.Thus, a Glucose load (e.g. oral Glucose tolerance test) is required in study participants with elevated FPG Concentration to accurately assess their future risk for T2DM, as well as their risk for CVD to identify the subgroup of IFG who are at greater risk and subject them to an intervention program to decrease their future T2DM and CVD risk.
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dapagliflozin lowers Plasma Glucose Concentration and improves β cell function
The Journal of Clinical Endocrinology and Metabolism, 2015Co-Authors: Aurora Merovci, Muhammad A Abdulghani, Giuseppe Daniele, Andrea Mari, Carolina Solis, Juan Xiong, Alberto Chavezvelazquez, Devjit Tripathy, Scheherezada Urban Mccarthy, Ralph A. DefronzoAbstract:Background: β-Cell dysfunction is a core defect in T2DM, and chronic, sustained hyperglycemia has been implicated in progressive β-cell failure, ie, glucotoxicity. The aim of the present study was to examine the effect of lowering the Plasma Glucose Concentration with dapagliflozin, a glucosuric agent, on β-cell function in T2DM individuals. Research Design and Methods: Twenty-four subjects with T2DM received dapagliflozin (n = 16) or placebo (n = 8) for 2 weeks, and a 75-g oral Glucose tolerance test (OGTT) and insulin clamp were performed before and after treatment. Plasma Glucose, insulin, and C-peptide Concentrations were measured during the OGTT. Results: Dapagliflozin significantly lowered both the fasting and 2-hour Plasma Glucose Concentrations and the incremental area under the Plasma Glucose Concentration curve (ΔG0–120) during OGTT by −33 ± 5 mg/dL, −73 ± 9 mg/dL, and −60 ± 12 mg/dL · min, respectively, compared to −13 ± 9, −33 ± 13, and −18 ± 9 reductions in placebo-treated subjects (both P < ...
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lowering Plasma Glucose Concentration by inhibiting renal sodium Glucose cotransport
Journal of Internal Medicine, 2014Co-Authors: Muhammad A Abdulghani, Ralph A. DefronzoAbstract:Maintaining normoglycaemia not only reduces the risk of diabetic microvascular complications but also corrects the metabolic abnormalities that contribute to the development and progression of hyperglycaemia, that is insulin resistance and beta-cell dysfunction. Progressive beta-cell failure, in addition to side effects associated with many current antidiabetic agents, for example hypoglycaemia and weight gain, presents major obstacles to the achievement of the recommended goal of glycaemic control in patients with type 2 diabetes mellitus (T2DM). Thus, novel effective therapies are needed for optimal Glucose control in subjects with T2DM. Most recently, specific inhibitors of the renal sodium–Glucose cotransporter 2 (SGLT2) have been developed to produce glucosuria and lower the Plasma Glucose Concentration. Because of the iR unique mechanism of action, which is independent of insulin secretion and insulin action, these agents are effective in lowering the Plasma Glucose Concentration in all stages of the disease and can be combined with all other antidiabetic agents. In this review, we will summarize the available data concerning the mechanism of action, efficacy and safety of this novel class of antidiabetic agents.
Philip E. Cryer - One of the best experts on this subject based on the ideXlab platform.
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evaluation and management of adult hypoglycemic disorders an endocrine society clinical practice guideline
The Journal of Clinical Endocrinology and Metabolism, 2009Co-Authors: Philip E. Cryer, Simon Heller, Lloyd Axelrod, Ashley B Grossman, Victor M Montori, Elizabeth R SeaquistAbstract:Objective: The aim is to provide guidelines for the evaluation and management of adults with hypoglycemic disorders, including those with diabetes mellitus. Evidence: Using the recommendations of the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) system, the quality of evidence is graded very low (⊕○○○), low (⊕⊕○○), moderate (⊕⊕⊕○), or high (⊕⊕⊕⊕). Conclusions: We recommend evaluation and management of hypoglycemia only in patients in whom Whipple’s triad—symptoms, signs, or both consistent with hypoglycemia, a low Plasma Glucose Concentration, and resolution of those symptoms or signs after the Plasma Glucose Concentration is raised—is documented. In patients with hypoglycemia without diabetes mellitus, we recommend the following strategy. First, pursue clinical clues to potential hypoglycemic etiologies—drugs, critical illnesses, hormone deficiencies, nonislet cell tumors. In the absence of these causes, the differential diagnosis narrows to accidental, surreptitious, or even...
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glucagon in concert with insulin supports the postabsorptive Plasma Glucose Concentration in humans
Diabetes, 2007Co-Authors: Suzanne M Breckenridge, Benjamin A Cooperberg, Ana Maria Arbelaez, Bruce W Patterson, Philip E. CryerAbstract:OBJECTIVE— Given the interest in glucagon antagonism as a potential treatment of diabetes, we tested the hypothesis that glucagon, in concert with insulin, supports the postabsorptive Plasma Glucose Concentration in humans. RESEARCH DESIGN AND METHODS— Following preliminary studies that indicated that a peripheral intravenous insulin dose of 0.1 mU · kg−1 · min−1 (lower than those used previously) provides basal insulin replacement and that a glucagon dose of 1.0 ng · kg−1 · min−1 underreplaces basal glucagon, we infused the somatostatin analog octreotide (30 ng · kg−1 · min−1) (with growth hormone replacement) over 4 h in 14 healthy adults on four separate occasions to produce endogenous insulin and glucagon deficiency with 1 ) saline (combined insulin and glucagon deficiency), 2 ) insulin replacement (isolated glucagon deficiency), 3 ) partial glucagon replacement (insulin and partial glucagon deficiency), and 4 ) insulin and partial glucagon replacement (partial glucagon deficiency). RESULTS— During combined insulin and glucagon deficiency, Glucose production decreased and then increased, and mean (±SE) Plasma Glucose decreased from 83 ± 1 to 63 ± 2 mg/dl at 60 min and then increased to 89 ± 3 mg/dl at 240 min. During isolated glucagon deficiency, Plasma Glucose decreased to hypoglycemic levels and was 55 ± 2 mg/dl at 240 min ( P < 0.0001 vs. combined insulin and glucagon deficiency). Partial glucagon replacement raised Plasma Glucose to higher levels ( P = 0.0469) during insulin deficiency and to higher levels ( P = 0.0090) during insulin replacement. CONCLUSIONS— These three findings provide direct evidence that glucagon, in concert with insulin, supports the postabsorptive Plasma Glucose Concentration in humans.
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maintenance of the postabsorptive Plasma Glucose Concentration insulin or insulin plus glucagon
American Journal of Physiology-endocrinology and Metabolism, 2005Co-Authors: Bharathi Raju, Philip E. CryerAbstract:The prevalent view is that the postabsorptive Plasma Glucose Concentration is maintained within the physiological range by the interplay of the Glucose-lowering action of insulin and the Glucose-ra...
Jukka Mustonen - One of the best experts on this subject based on the ideXlab platform.
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the clinical presentation of puumala hantavirus induced hemorrhagic fever with renal syndrome is related to Plasma Glucose Concentration
Viruses, 2021Co-Authors: Johanna Tietäväinen, Satu Mäkelä, Heini Huhtala, Ilkka H. Pörsti, Tomas Strandin, Antti Vaheri, Jukka MustonenAbstract:Puumala hantavirus (PUUV) causes a hemorrhagic fever with renal syndrome characterized by thrombocytopenia, increased capillary leakage, and acute kidney injury (AKI). As glucosuria at hospital admission predicts the severity of PUUV infection, we explored how Plasma Glucose Concentration associates with disease severity. Plasma Glucose values were measured during hospital care in 185 patients with PUUV infection. They were divided into two groups according to maximum Plasma Glucose Concentration: P-Gluc < 7.8 mmol/L (n = 134) and P-Gluc ≥ 7.8 mmol/L (n = 51). The determinants of disease severity were analyzed across groups. Patients with P-Gluc ≥7.8 mmol/L had higher hematocrit (0.46 vs. 0.43; p < 0.001) and lower Plasma albumin Concentration (24 vs. 29 g/L; p < 0.001) than patients with P-Gluc < 7.8 mmol/L. They presented with higher prevalence of pulmonary infiltrations and pleural effusion in chest radiograph, higher prevalence of shock and greater weight change during hospitalization. Patients with P-Gluc ≥ 7.8 mmol/L were characterized by lower platelet count (50 vs. 66 × 109/L; p = 0.001), more severe AKI (Plasma creatinine 272 vs. 151 µmol/L; p = 0.001), and longer hospital treatment (8 vs. 6 days; p < 0.001) than patients with P-Gluc < 7.8 mmol/L. Plasma Glucose level is associated with the severity of capillary leakage, thrombocytopenia, inflammation, and AKI in patients with acute PUUV infection.
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The Clinical Presentation of Puumala Hantavirus Induced Hemorrhagic Fever with Renal Syndrome Is Related to Plasma Glucose Concentration
'MDPI AG', 2021Co-Authors: Johanna Tietäväinen, Satu Mäkelä, Heini Huhtala, Ilkka H. Pörsti, Tomas Strandin, Antti Vaheri, Jukka MustonenAbstract:Puumala hantavirus (PUUV) causes a hemorrhagic fever with renal syndrome characterized by thrombocytopenia, increased capillary leakage, and acute kidney injury (AKI). As glucosuria at hospital admission predicts the severity of PUUV infection, we explored how Plasma Glucose Concentration associates with disease severity. Plasma Glucose values were measured during hospital care in 185 patients with PUUV infection. They were divided into two groups according to maximum Plasma Glucose Concentration: P-Gluc n = 134) and P-Gluc ≥ 7.8 mmol/L (n = 51). The determinants of disease severity were analyzed across groups. Patients with P-Gluc ≥7.8 mmol/L had higher hematocrit (0.46 vs. 0.43; p p 9/L; p = 0.001), more severe AKI (Plasma creatinine 272 vs. 151 µmol/L; p = 0.001), and longer hospital treatment (8 vs. 6 days; p < 0.001) than patients with P-Gluc < 7.8 mmol/L. Plasma Glucose level is associated with the severity of capillary leakage, thrombocytopenia, inflammation, and AKI in patients with acute PUUV infection
Leif Groop - One of the best experts on this subject based on the ideXlab platform.
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the shape of Plasma Glucose Concentration curve during ogtt predicts future risk of type 2 diabetes
Diabetes-metabolism Research and Reviews, 2010Co-Authors: Muhammad A Abdulghani, Tiinamaija Tuomi, Valeriya Lyssenko, Ralph A. Defronzo, Leif GroopAbstract:Background The aim of the study is to assess the relationship between the shape of Plasma Glucose Concentration during the OGTT and future risk for T2DM. Methods 2445 non-diabetic subjects from the Botnia study received an OGTT at baseline and after 7-8 years of follow-up. Results NGT and IFG subjects who returned their Plasma Glucose Concentration following an ingested Glucose load below FPG within 60 min had increased insulin sensitivity, greater insulin secretion and lower risk for future T2DM compared to NGT and IFG subjects whose post-load Plasma Glucose Concentration required 120 min or longer to return their Plasma Glucose level to FPG level. IGT subjects who had a lower Plasma Glucose Concentration at 1-h compared to 2-h during oGrr had greater insulin sensitivity, better beta cell function and lower risk for future T2DM. Conclusions These data suggest that the shape of Glucose curve can be utilized to assess future risk for T2DM. Copyright (C) 2010 John Wiley & Sons, Ltd.
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fasting versus postload Plasma Glucose Concentration and the risk for future type 2 diabetes results from the botnia study
Diabetes Care, 2009Co-Authors: Muhammad A Abdulghani, Tiinamaija Tuomi, Valeriya Lyssenko, Ralph A. Defronzo, Leif GroopAbstract:OBJECTIVE—The purpose of this study was to assess the efficacy of the postload Plasma Glucose Concentration in predicting future risk of type 2 diabetes, compared with prediction models based on measurement of the fasting Plasma Glucose (FPG) Concentration. RESEARCH DESIGN AND METHODS—A total of 2,442 subjects from the Botnia Study, who were free of type 2 diabetes at baseline, received an oral Glucose tolerance test (OGTT) at baseline and after 7–8 years of follow-up. Future risk for type 2 diabetes was assessed with area under the receiver-operating characteristic curve for prediction models based up measurement of the FPG Concentration 1) with or without a 1-h Plasma Glucose Concentration during the OGTT and 2) with or without the metabolic syndrome. RESULTS—Prediction models based on measurement of the FPG Concentration were weak predictors for the risk of future type 2 diabetes. Addition of a 1-h Plasma Glucose Concentration markedly enhanced prediction of the risk of future type 2 diabetes. A cut point of 155 mg/dl for the 1-h Plasma Glucose Concentration during the OGTT and presence of the metabolic syndrome were used to stratify subjects in each Glucose tolerance group into low, intermediate, and high risk for future type 2 diabetes. CONCLUSIONS—The Plasma Glucose Concentration at 1 h during the OGTT is a strong predictor of future risk for type 2 diabetes and adds to the prediction power of models based on measurements made during the fasting state. A Plasma Glucose cut point of 155 mg/dl plus the Adult Treatment Panel III criteria for the metabolic syndrome can be used to stratify nondiabetic subjects into low-, intermediate-, and high-risk groups.