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John E. Gerich

Researcher at University of Rochester

Publications -  177
Citations -  19283

John E. Gerich is an academic researcher from University of Rochester. The author has contributed to research in topics: Insulin & Diabetes mellitus. The author has an hindex of 66, co-authored 177 publications receiving 18454 citations. Previous affiliations of John E. Gerich include University of Rochester Medical Center & University of Tübingen.

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The Treat-to-Target Trial: Randomized addition of glargine or human NPH insulin to oral therapy of type 2 diabetic patients

TL;DR: Systematically titrating bedtime basal insulin added to oral therapy can safely achieve 7% HbA(1c) in a majority of overweight patients with type 2 diabetes, thus reducing a leading barrier to initiating insulin.
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Metabolic effects of metformin in non-insulin-dependent diabetes mellitus.

TL;DR: Metformin acts primarily by decreasing hepatic glucose output, largely by inhibiting gluconeogenesis, and also seems to induce weight loss, preferentially involving adipose tissue.
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Efficacy and safety of the human glucagon-like peptide-1 analog liraglutide in combination with metformin and thiazolidinedione in patients with type 2 diabetes (LEAD-4 Met+TZD).

TL;DR: Liraglutide combined with metformin and a thiazolidinedione is a well-tolerated combination therapy for type 2 diabetes, providing significant improvements in glycemic control and C-peptide and homeostasis model assessment of β-cell function.
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Dose-response characteristics for effects of insulin on production and utilization of glucose in man

TL;DR: The above dose-response relationships indicate that in man glucose production is more sensitive to changes in plasma insulin concentration than is glucose utilization; both hepatic and peripheral tissues may contain "spare" insulin receptors; and relatively minor changes in Plasma insulin concentration or insulin receptor function can cause appreciable alterations in glucose metabolism.
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Role of Reduced Suppression of Glucose Production and Diminished Early Insulin Release in Impaired Glucose Tolerance

TL;DR: Impaired glucose tolerance, the precursor of NIDDM, results primarily from reduced suppression of hepatic glucose output due to abnormal pancreatic islet-cell function.