Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10747899 | Biochemical and Biophysical Research Communications | 2016 | 5 Pages |
Abstract
Replication initiator 1 (Repin1) is a zinc finger protein playing a role in insulin sensitivity, body fat mass and lipid metabolism by regulating the expression key genes of glucose and lipid metabolism. Here, we tested the hypothesis that introgression of a Repin1 deletion into db/db mice improves glucose metabolism in vivo. We generated a whole body Repin1 deficient db/db double knockout mouse (Rep1â/âx db/db) and systematically characterized the consequences of Repin1 deficiency on insulin sensitivity, glucose and lipid metabolism parameters and fat mass. Hyperinsulinemic-euglycemic clamp studies revealed significantly improved insulin sensitivity in Rep1â/âx db/db mice, which are also characterized by lower HbA1c, lower body fat mass and reduced adipose tissue (AT) inflammation area. Our study provides evidence that loss of Repin1 in db/db mice improves insulin sensitivity and reduces chronic hyperglycemia most likely by reducing fat mass and AT inflammation.
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Authors
Anne Kunath, Nico Hesselbarth, Martin Gericke, Matthias Kern, Sebastian Dommel, Peter Kovacs, Michael Stumvoll, Matthias Blüher, Nora Klöting,