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Jens J Holst - One of the best experts on this subject based on the ideXlab platform.

  • linagliptin a xanthine based Dipeptidyl peptidase 4 Inhibitor with an unusual profile for the treatment of type 2 diabetes
    Expert Opinion on Investigational Drugs, 2010
    Co-Authors: Carolyn F Deacon, Jens J Holst
    Abstract:

    Importance of the field: Type 2 diabetes is a progressive disease for which current treatments are often unsatisfactory with respect to achieving therapeutic goals and unwanted side effects.Areas covered: Preclinical and clinical studies of linagliptin, a new oral antidiabetic agent, including data presented at Scientific Meetings and peer-reviewed studies published since 2007.What the reader will gain: This article reviews pharmacokinetic and pharmacodynamic characteristics of linagliptin. Linagliptin belongs to a new chemical class of Dipeptidyl pepidase-4 (DPP-4) Inhibitors, which comprise xanthine-based compounds. It is a potent, long-acting Inhibitor with high selectivity for DPP-4 versus the related enzymes DPP-8 and DPP-9. The drug has modest oral availability in humans, but is absorbed rapidly to inhibit plasma DPP-4 activity by > 80% over 24 h. It is not metabolized appreciably in vivo, but binds extensively to plasma proteins, with elimination occurring primarily in the liver. Linagliptin reduce...

  • measurements of islet function and glucose metabolism with the Dipeptidyl peptidase 4 Inhibitor vildagliptin in patients with type 2 diabetes
    The Journal of Clinical Endocrinology and Metabolism, 2008
    Co-Authors: Koichiro Azuma, Jens J Holst, Carolyn F Deacon, Zofia Radikova, Juliet Mancino, Frederico G S Toledo, Ernestine Thomas, Cyrous Kangani, Claudio Cobelli, Yanling He
    Abstract:

    Objective: Pharmacological inhibition with the Dipeptidyl peptidase 4 (DPP-4) Inhibitor vildagliptin prolongs the action of endogenously secreted incretin hormones leading to improved glycemic control in patients with type 2 diabetes mellitus (T2DM). We undertook a double-blinded, randomized-order, crossover study to examine the vildagliptin mechanisms of action on islet function and glucose utilization. Research Design and Methods: Participants with T2DM (n = 16) who had a baseline hemoglobin A1c of 7.1 ± 0.2% completed a crossover study with 6 wk of treatment with vildagliptin and 6 wk with placebo. At the completion of each arm, participants had a study of postprandial metabolism and a two-step glucose clamp performed at 20 and 80 mU/min·m2 insulin infusions. Results: Vildagliptin increased postprandial glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide by 3- and 2-fold, respectively, reduced fasting plasma glucose and postprandial plasma glucose by 1.3 ± 0.3 mmol/liter and 1.6 ± ...

  • the Dipeptidyl peptidase 4 Inhibitor vildagliptin improves β cell function and insulin sensitivity in subjects with impaired fasting glucose
    Diabetes Care, 2008
    Co-Authors: Kristina M Utzschneider, James E Foley, Jenny Tong, Brenda Montgomery, Jayalakshmi Udayasankar, Fernando Gerchman, Santica M Marcovina, Catherine Watson, Monica Liguerossaylan, Jens J Holst
    Abstract:

    OBJECTIVE —To evaluate the effect of treatment with the Dipeptidyl peptidase (DPP)-4 Inhibitor vildagliptin on insulin sensitivity and β-cell function in subjects with impaired fasting glucose (IFG). RESEARCH DESIGN AND METHODS —A total of 22 subjects with IFG (11 female and 11 male, mean ± SD age 59.6 ± 11.5 years) were treated orally with 100 mg vildagliptin once daily in a single-blind study. Subjects received placebo for 2 weeks (run-in) followed by vildagliptin for 6 weeks (treatment) and then placebo for 2 weeks (washout). A frequently sampled intravenous glucose tolerance test (FSIGT), followed by a 2-h meal tolerance test (MTT), was performed at 2, 8, and 10 weeks. From the FSIGT, the acute insulin response to glucose (AIR g ) and insulin sensitivity index ( S I ) were determined and used to compute the disposition index (AIR g × S I ) as a measure of β-cell function. RESULTS —Fasting plasma glucose did not change after 6 weeks of vildagliptin treatment. With treatment, mean ± SEM AIR g increased from 224 ± 44 to 286 ± 52 pmol/l ( P S I improved from 2.8 ± 0.5 to 3.5 ± 0.5 × 10 −5 · min −1 · pmol −1 · l ( P −5 /min ( P −1 · min −1 ; P = 0.002), but this effect was not sustained after washout. CONCLUSIONS —The DPP-4 Inhibitor vildagliptin improves insulin sensitivity and β-cell function, leading to improved postprandial glycemia in subjects with IFG, who are known to have β-cell dysfunction. Thus, vildagliptin may prevent progression to diabetes in high-risk subjects.

James E Foley - One of the best experts on this subject based on the ideXlab platform.

  • vildagliptin reduces glucagon during hyperglycemia and sustains glucagon counterregulation during hypoglycemia in type 1 diabetes
    The Journal of Clinical Endocrinology and Metabolism, 2012
    Co-Authors: Johan Farngren, James E Foley, Anja Schweizer, Margaretha Persson, Bo Ahrén
    Abstract:

    Context: The Dipeptidyl Peptidase-4 Inhibitor, vildagliptin, inhibits glucagon secretion at hyperglycemia but appears to enhance glucagon counterregulation during hypoglycemia in type 2 diabetes. Objective: The objective of the investigation was to study whether vildagliptin also improves α-cell function in type 1 diabetes (T1D). Patients and Methods: The study was a single-center, double-blind, randomized, placebo-controlled crossover study involving 28 patients with C-peptide negative and antibody positive T1D [21 males, seven females, glycosylated hemoglobin 57.9 mmol/mol (7.5%)]. Patients received vildagliptin (50 mg twice a day) or placebo as an add-on to their insulin therapy for 4 wk each. On d 28 of the respective treatment period, patients were served a standard meal (500 kcal) to raise the circulating incretin hormone levels followed by a hyperinsulinemic hypoglycemic clamp at 2.5 mmol/liter. Main Outcome Measure: The increase in plasma glucagon levels during the 30-min hypoglycemic clamp (min 1...

  • Evidence to support the use of vildagliptin monotherapy in the treatment of type 2 diabetes mellitus.
    Vascular Health and Risk Management, 2012
    Co-Authors: Sylvie Dejager, Anja Schweizer, James E Foley
    Abstract:

    The efficacy and safety of the Dipeptidyl Peptidase-4 Inhibitor, vildagliptin, as monotherapy have been widely confirmed in a large body of clinical studies of up to 2 years’ duration in various populations with type 2 diabetes mellitus. This paper reviews the data supporting the use of vildagliptin in monotherapy. Consideration based on baseline glycated hemoglobin levels and age is given to patient segments where metformin is not appropriate. In addition, although prediabetes is not an indication, this manuscript briefly reviews some of the existing data showing that the mechanisms at work in diabetic populations are active in patients currently classified as prediabetic, with impaired glucose tolerance or impaired fasting glucose. Finally, the rationale for vildagliptin dosing frequency in monotherapy is discussed. In summary, this review aims to define where in community practice the use of vildagliptin as monotherapy is most desirable, focusing on segments of the population with type 2 diabetes mellitus that might receive the greatest benefit from vildagliptin in the management of their disease.

  • mechanisms of action of the Dipeptidyl peptidase 4 Inhibitor vildagliptin in humans
    Diabetes Obesity and Metabolism, 2011
    Co-Authors: Bo Ahrén, Anja Schweizer, B E Dunning, Sylvie Dejager, Edwin Bernard Villhauer, James E Foley
    Abstract:

    Inhibition of Dipeptidyl Peptidase-4 (DPP-4) by vildagliptin prevents degradation of glucagon-like peptide-1 (GLP-1) and reduces glycemia in type 2 diabetes, with low risk for hypoglycemia and no weight gain. Vildagliptin binds covalently to the catalytic site of DPP-4, eliciting prolonged enzyme inhibition. This raises intact GLP-1 levels, both after meal ingestion and in the fasting state. Vildagliptin has been shown to stimulate insulin secretion and to inhibit glucagon secretion in a glucose-dependent manner. At hypoglycemic levels, the counterregulatory glucagon response is enhanced relative to baseline by vildagliptin. Vildagliptin also inhibits hepatic glucose production, mainly through changes in islet hormone secretion, and improves insulin sensitivity, as determined with a variety of methods. These effects underlie the improved glycemia with low risk for hypoglycemia. Vildagliptin also suppresses postprandial triglyceride-rich lipoprotein levels after ingestion of a fat-rich meal and reduces fasting lipolysis, suggesting inhibition of fat absorption and reduced triglyceride stores in non-fat tissues. The large body of knowledge on vildagliptin regarding enzyme binding, incretin and islet hormone secretion and glucose and lipid metabolism is summarized, with discussion of the integrated mechanisms and comparison with other DPP-4 Inhibitors and GLP-1 receptor activators, where appropriate.

  • changes in prandial glucagon levels after a 2 year treatment with vildagliptin or glimepiride in patients with type 2 diabetes inadequately controlled with metformin monotherapy
    Diabetes Care, 2010
    Co-Authors: Bo Ahrén, James E Foley, Sylvie Dejager, Eleuterio Ferrannini, Bernard Zinman, David R Matthews, Vivian Fonseca
    Abstract:

    OBJECTIVE: To determine if the Dipeptidyl Peptidase-4 Inhibitor vildagliptin more effectively inhibits glucagon levels than the sulfonylurea glimepiride during a meal. RESEARCH DESIGN AND METHODS: Glucagon responses to a standard meal were measured at baseline and study end point (mean 1.8 years) in a trial evaluating add-on therapy to metformin with 50 mg vildagliptin b.i.d. compared with glimepiride up to 6 mg q.d. in type 2 diabetes (baseline A1C 7.3 +/- 0.6%). RESULTS: A1C and prandial glucose area under the curve (AUC)(0-2 h) were reduced similarly in both groups, whereas prandial insulin AUC(0-2 h) increased to a greater extent by glimepiride. Prandial glucagon AUC(0-2 h) (baseline 66.6 +/- 2.3 pmol . h(-1) . l(-1)) decreased by 3.4 +/- 1.6 pmol . h(-1) . l(-1) by vildagliptin (n = 137) and increased by 3.8 +/- 1.7 pmol . h(-1) . l(-1) by glimepiride (n = 121). The between-group difference was 7.3 +/- 2.1 pmol . h(-1) . l(-1) (P < 0.001). CONCLUSIONS: Vildagliptin therapy but not glimepiride improves postprandial alpha-cell function, which persists for at least 2 years.

  • treatment with the Dipeptidyl peptidase 4 Inhibitor vildagliptin improves fasting islet cell function in subjects with type 2 diabetes
    The Journal of Clinical Endocrinology and Metabolism, 2009
    Co-Authors: David A Dalessio, B E Dunning, Amanda M Denney, Linda M Hermiller, Ronald L Prigeon, Julie M Martin, William G Tharp, Monica Liqueros Saylan, Yanling He, James E Foley
    Abstract:

    Context: Dipeptidyl peptidase 4 (DPP-4) Inhibitors are proposed to lower blood glucose in type 2 diabetes mellitus (T2DM) by prolonging the activity of the circulating incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1). Consistent with this mechanism of action, DPP-4 Inhibitors improve glucose tolerance after meals by increasing insulin and reducing glucagon levels in the plasma. However, DPP-4 Inhibitors also reduce fasting blood glucose, an unexpected effect because circulating levels of active GIP and GLP-1 are low in the postabsorptive state. Objective: The objective of the study was to examine the effects of DPP-4 inhibition on fasting islet function. Design: We conducted a randomized, double-blind, placebo-controlled trial. Setting: The study was performed in General Clinical Research Centers at two University Hospitals. Subjects: Forty-one subjects with T2DM were treated with metformin or diet, having good glycemic control with glycosylated hemoglobin ...

Carolyn F Deacon - One of the best experts on this subject based on the ideXlab platform.

  • linagliptin a xanthine based Dipeptidyl peptidase 4 Inhibitor with an unusual profile for the treatment of type 2 diabetes
    Expert Opinion on Investigational Drugs, 2010
    Co-Authors: Carolyn F Deacon, Jens J Holst
    Abstract:

    Importance of the field: Type 2 diabetes is a progressive disease for which current treatments are often unsatisfactory with respect to achieving therapeutic goals and unwanted side effects.Areas covered: Preclinical and clinical studies of linagliptin, a new oral antidiabetic agent, including data presented at Scientific Meetings and peer-reviewed studies published since 2007.What the reader will gain: This article reviews pharmacokinetic and pharmacodynamic characteristics of linagliptin. Linagliptin belongs to a new chemical class of Dipeptidyl pepidase-4 (DPP-4) Inhibitors, which comprise xanthine-based compounds. It is a potent, long-acting Inhibitor with high selectivity for DPP-4 versus the related enzymes DPP-8 and DPP-9. The drug has modest oral availability in humans, but is absorbed rapidly to inhibit plasma DPP-4 activity by > 80% over 24 h. It is not metabolized appreciably in vivo, but binds extensively to plasma proteins, with elimination occurring primarily in the liver. Linagliptin reduce...

  • measurements of islet function and glucose metabolism with the Dipeptidyl peptidase 4 Inhibitor vildagliptin in patients with type 2 diabetes
    The Journal of Clinical Endocrinology and Metabolism, 2008
    Co-Authors: Koichiro Azuma, Jens J Holst, Carolyn F Deacon, Zofia Radikova, Juliet Mancino, Frederico G S Toledo, Ernestine Thomas, Cyrous Kangani, Claudio Cobelli, Yanling He
    Abstract:

    Objective: Pharmacological inhibition with the Dipeptidyl peptidase 4 (DPP-4) Inhibitor vildagliptin prolongs the action of endogenously secreted incretin hormones leading to improved glycemic control in patients with type 2 diabetes mellitus (T2DM). We undertook a double-blinded, randomized-order, crossover study to examine the vildagliptin mechanisms of action on islet function and glucose utilization. Research Design and Methods: Participants with T2DM (n = 16) who had a baseline hemoglobin A1c of 7.1 ± 0.2% completed a crossover study with 6 wk of treatment with vildagliptin and 6 wk with placebo. At the completion of each arm, participants had a study of postprandial metabolism and a two-step glucose clamp performed at 20 and 80 mU/min·m2 insulin infusions. Results: Vildagliptin increased postprandial glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide by 3- and 2-fold, respectively, reduced fasting plasma glucose and postprandial plasma glucose by 1.3 ± 0.3 mmol/liter and 1.6 ± ...

Sylvie Dejager - One of the best experts on this subject based on the ideXlab platform.

  • Evidence to support the use of vildagliptin monotherapy in the treatment of type 2 diabetes mellitus.
    Vascular Health and Risk Management, 2012
    Co-Authors: Sylvie Dejager, Anja Schweizer, James E Foley
    Abstract:

    The efficacy and safety of the Dipeptidyl Peptidase-4 Inhibitor, vildagliptin, as monotherapy have been widely confirmed in a large body of clinical studies of up to 2 years’ duration in various populations with type 2 diabetes mellitus. This paper reviews the data supporting the use of vildagliptin in monotherapy. Consideration based on baseline glycated hemoglobin levels and age is given to patient segments where metformin is not appropriate. In addition, although prediabetes is not an indication, this manuscript briefly reviews some of the existing data showing that the mechanisms at work in diabetic populations are active in patients currently classified as prediabetic, with impaired glucose tolerance or impaired fasting glucose. Finally, the rationale for vildagliptin dosing frequency in monotherapy is discussed. In summary, this review aims to define where in community practice the use of vildagliptin as monotherapy is most desirable, focusing on segments of the population with type 2 diabetes mellitus that might receive the greatest benefit from vildagliptin in the management of their disease.

  • mechanisms of action of the Dipeptidyl peptidase 4 Inhibitor vildagliptin in humans
    Diabetes Obesity and Metabolism, 2011
    Co-Authors: Bo Ahrén, Anja Schweizer, B E Dunning, Sylvie Dejager, Edwin Bernard Villhauer, James E Foley
    Abstract:

    Inhibition of Dipeptidyl Peptidase-4 (DPP-4) by vildagliptin prevents degradation of glucagon-like peptide-1 (GLP-1) and reduces glycemia in type 2 diabetes, with low risk for hypoglycemia and no weight gain. Vildagliptin binds covalently to the catalytic site of DPP-4, eliciting prolonged enzyme inhibition. This raises intact GLP-1 levels, both after meal ingestion and in the fasting state. Vildagliptin has been shown to stimulate insulin secretion and to inhibit glucagon secretion in a glucose-dependent manner. At hypoglycemic levels, the counterregulatory glucagon response is enhanced relative to baseline by vildagliptin. Vildagliptin also inhibits hepatic glucose production, mainly through changes in islet hormone secretion, and improves insulin sensitivity, as determined with a variety of methods. These effects underlie the improved glycemia with low risk for hypoglycemia. Vildagliptin also suppresses postprandial triglyceride-rich lipoprotein levels after ingestion of a fat-rich meal and reduces fasting lipolysis, suggesting inhibition of fat absorption and reduced triglyceride stores in non-fat tissues. The large body of knowledge on vildagliptin regarding enzyme binding, incretin and islet hormone secretion and glucose and lipid metabolism is summarized, with discussion of the integrated mechanisms and comparison with other DPP-4 Inhibitors and GLP-1 receptor activators, where appropriate.

  • Minimizing the risk of hypoglycemia with vildagliptin: Clinical experience, mechanistic basis, and importance in type 2 diabetes management
    Diabetes Therapy, 2011
    Co-Authors: Sylvie Dejager, Anja Schweizer
    Abstract:

    Even if the true incidence of hypoglycemia in type 2 diabetes mellitus (T2DM) remains difficult to estimate, with highly variable rates reported in the literature, it is likely more common than previously thought. While most hypoglycemic episodes in T2DM are considered “mild,” they still have a substantial clinical impact. Severe hypoglycemia also exists in T2DM, with recent landmark studies prompting much debate about the potential role of severe hypoglycemia in cardiovascular morbidity and mortality, even though there is currently no definitive evidence for causality. The challenge in the treatment of T2DM remains the achievement of optimal glycemic control to lower the risk for long-term complications while avoiding hypoglycemia. Successful treatment strategies should therefore include careful selection of therapies to prevent hypoglycemia, starting early in the disease management process, in order to best preserve counterregulation. The Dipeptidyl Peptidase-4 Inhibitor, vildagliptin, is a good treatment option to minimize the risk of hypoglycemia over time, while maintaining good glucose control. Extensive clinical experience is available for vildagliptin, with data published for all stages of the condition and with the low hypoglycemic potential stemming from a solid mechanistic basis.

  • changes in prandial glucagon levels after a 2 year treatment with vildagliptin or glimepiride in patients with type 2 diabetes inadequately controlled with metformin monotherapy
    Diabetes Care, 2010
    Co-Authors: Bo Ahrén, James E Foley, Sylvie Dejager, Eleuterio Ferrannini, Bernard Zinman, David R Matthews, Vivian Fonseca
    Abstract:

    OBJECTIVE: To determine if the Dipeptidyl Peptidase-4 Inhibitor vildagliptin more effectively inhibits glucagon levels than the sulfonylurea glimepiride during a meal. RESEARCH DESIGN AND METHODS: Glucagon responses to a standard meal were measured at baseline and study end point (mean 1.8 years) in a trial evaluating add-on therapy to metformin with 50 mg vildagliptin b.i.d. compared with glimepiride up to 6 mg q.d. in type 2 diabetes (baseline A1C 7.3 +/- 0.6%). RESULTS: A1C and prandial glucose area under the curve (AUC)(0-2 h) were reduced similarly in both groups, whereas prandial insulin AUC(0-2 h) increased to a greater extent by glimepiride. Prandial glucagon AUC(0-2 h) (baseline 66.6 +/- 2.3 pmol . h(-1) . l(-1)) decreased by 3.4 +/- 1.6 pmol . h(-1) . l(-1) by vildagliptin (n = 137) and increased by 3.8 +/- 1.7 pmol . h(-1) . l(-1) by glimepiride (n = 121). The between-group difference was 7.3 +/- 2.1 pmol . h(-1) . l(-1) (P < 0.001). CONCLUSIONS: Vildagliptin therapy but not glimepiride improves postprandial alpha-cell function, which persists for at least 2 years.

Anja Schweizer - One of the best experts on this subject based on the ideXlab platform.

  • vildagliptin reduces glucagon during hyperglycemia and sustains glucagon counterregulation during hypoglycemia in type 1 diabetes
    The Journal of Clinical Endocrinology and Metabolism, 2012
    Co-Authors: Johan Farngren, James E Foley, Anja Schweizer, Margaretha Persson, Bo Ahrén
    Abstract:

    Context: The Dipeptidyl Peptidase-4 Inhibitor, vildagliptin, inhibits glucagon secretion at hyperglycemia but appears to enhance glucagon counterregulation during hypoglycemia in type 2 diabetes. Objective: The objective of the investigation was to study whether vildagliptin also improves α-cell function in type 1 diabetes (T1D). Patients and Methods: The study was a single-center, double-blind, randomized, placebo-controlled crossover study involving 28 patients with C-peptide negative and antibody positive T1D [21 males, seven females, glycosylated hemoglobin 57.9 mmol/mol (7.5%)]. Patients received vildagliptin (50 mg twice a day) or placebo as an add-on to their insulin therapy for 4 wk each. On d 28 of the respective treatment period, patients were served a standard meal (500 kcal) to raise the circulating incretin hormone levels followed by a hyperinsulinemic hypoglycemic clamp at 2.5 mmol/liter. Main Outcome Measure: The increase in plasma glucagon levels during the 30-min hypoglycemic clamp (min 1...

  • Evidence to support the use of vildagliptin monotherapy in the treatment of type 2 diabetes mellitus.
    Vascular Health and Risk Management, 2012
    Co-Authors: Sylvie Dejager, Anja Schweizer, James E Foley
    Abstract:

    The efficacy and safety of the Dipeptidyl Peptidase-4 Inhibitor, vildagliptin, as monotherapy have been widely confirmed in a large body of clinical studies of up to 2 years’ duration in various populations with type 2 diabetes mellitus. This paper reviews the data supporting the use of vildagliptin in monotherapy. Consideration based on baseline glycated hemoglobin levels and age is given to patient segments where metformin is not appropriate. In addition, although prediabetes is not an indication, this manuscript briefly reviews some of the existing data showing that the mechanisms at work in diabetic populations are active in patients currently classified as prediabetic, with impaired glucose tolerance or impaired fasting glucose. Finally, the rationale for vildagliptin dosing frequency in monotherapy is discussed. In summary, this review aims to define where in community practice the use of vildagliptin as monotherapy is most desirable, focusing on segments of the population with type 2 diabetes mellitus that might receive the greatest benefit from vildagliptin in the management of their disease.

  • mechanisms of action of the Dipeptidyl peptidase 4 Inhibitor vildagliptin in humans
    Diabetes Obesity and Metabolism, 2011
    Co-Authors: Bo Ahrén, Anja Schweizer, B E Dunning, Sylvie Dejager, Edwin Bernard Villhauer, James E Foley
    Abstract:

    Inhibition of Dipeptidyl Peptidase-4 (DPP-4) by vildagliptin prevents degradation of glucagon-like peptide-1 (GLP-1) and reduces glycemia in type 2 diabetes, with low risk for hypoglycemia and no weight gain. Vildagliptin binds covalently to the catalytic site of DPP-4, eliciting prolonged enzyme inhibition. This raises intact GLP-1 levels, both after meal ingestion and in the fasting state. Vildagliptin has been shown to stimulate insulin secretion and to inhibit glucagon secretion in a glucose-dependent manner. At hypoglycemic levels, the counterregulatory glucagon response is enhanced relative to baseline by vildagliptin. Vildagliptin also inhibits hepatic glucose production, mainly through changes in islet hormone secretion, and improves insulin sensitivity, as determined with a variety of methods. These effects underlie the improved glycemia with low risk for hypoglycemia. Vildagliptin also suppresses postprandial triglyceride-rich lipoprotein levels after ingestion of a fat-rich meal and reduces fasting lipolysis, suggesting inhibition of fat absorption and reduced triglyceride stores in non-fat tissues. The large body of knowledge on vildagliptin regarding enzyme binding, incretin and islet hormone secretion and glucose and lipid metabolism is summarized, with discussion of the integrated mechanisms and comparison with other DPP-4 Inhibitors and GLP-1 receptor activators, where appropriate.

  • Minimizing the risk of hypoglycemia with vildagliptin: Clinical experience, mechanistic basis, and importance in type 2 diabetes management
    Diabetes Therapy, 2011
    Co-Authors: Sylvie Dejager, Anja Schweizer
    Abstract:

    Even if the true incidence of hypoglycemia in type 2 diabetes mellitus (T2DM) remains difficult to estimate, with highly variable rates reported in the literature, it is likely more common than previously thought. While most hypoglycemic episodes in T2DM are considered “mild,” they still have a substantial clinical impact. Severe hypoglycemia also exists in T2DM, with recent landmark studies prompting much debate about the potential role of severe hypoglycemia in cardiovascular morbidity and mortality, even though there is currently no definitive evidence for causality. The challenge in the treatment of T2DM remains the achievement of optimal glycemic control to lower the risk for long-term complications while avoiding hypoglycemia. Successful treatment strategies should therefore include careful selection of therapies to prevent hypoglycemia, starting early in the disease management process, in order to best preserve counterregulation. The Dipeptidyl Peptidase-4 Inhibitor, vildagliptin, is a good treatment option to minimize the risk of hypoglycemia over time, while maintaining good glucose control. Extensive clinical experience is available for vildagliptin, with data published for all stages of the condition and with the low hypoglycemic potential stemming from a solid mechanistic basis.