J
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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Journal ArticleDOI
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.
Journal ArticleDOI
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).
Bernard Zinman,John E. Gerich,John B. Buse,Andrew Lewin,Sherwyn Schwartz,Philip Raskin,Paula M Hale,Milan Zdravkovic,Lawrence Blonde +8 more
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
Asimina Mitrakou,David E. Kelley,Marian Mokan,Thiemo Veneman,Thomas Pangburn,James J. Reilly,John E. Gerich +6 more
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.