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David Holmes

Researcher at Novartis

Publications -  5
Citations -  1319

David Holmes is an academic researcher from Novartis. The author has contributed to research in topics: Type 2 diabetes & Insulin. The author has an hindex of 4, co-authored 5 publications receiving 1280 citations.

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Journal ArticleDOI

Inhibition of Dipeptidyl Peptidase-4 Reduces Glycemia, Sustains Insulin Levels, and Reduces Glucagon Levels in Type 2 Diabetes

TL;DR: Improved metabolic control by DPP-4 inhibition in type 2 diabetes is seen in association with reduced glucagon levels and, despite the lower glycemia, unaltered insulin levels.
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Inhibition of dipeptidyl peptidase IV improves metabolic control over a 4-week study period in type 2 diabetes.

TL;DR: In inhibition of DPP IV is a feasible approach to the treatment of type 2 diabetes in the early stage of the disease, as concluded in a placebo-controlled double-blind multicenter study.
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The dipeptidyl peptidase 4 inhibitor vildagliptin does not accentuate glibenclamide-induced hypoglycemia but reduces glucose-induced glucagon-like peptide 1 and gastric inhibitory polypeptide secretion.

TL;DR: Sulfonylurea-induced hypoglycemia after the oral administration of glibenclamide is not accentuated by the coadministration of vildagliptin, and may be explained by a negative feedback regulation of GLP-1 and GIP secretion that limits the degree to which the active incretin levels are enhanced.
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Efficacy and safety of nateglinide in type 2 diabetic patients with modest fasting hyperglycemia.

TL;DR: Nateglinide is a safe and effective therapeutic option for treatment of patients with mild to moderate fasting hyperglycemia and elicited a dose-dependent reduction of placebo-adjusted hemoglobin A(1c) and FPG.
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Comparison of the postprandial glucose and insulin profiles with nateglinide and gliclazide in type 2 diabetic patients

TL;DR: Nateglinide was more effective than gliclazide over an extended postprandial period in type 2 diabetic patients and was associated with earlier, higher and shorter-lived insulin and proinsulin secretory responses.