Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 111, Issue 2, Pages 225-230Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200316521
Keywords
-
Categories
Funding
- NIDDK NIH HHS [R01 DK055758, R01 DK-55758, R01 DK048321, R01 DK-48321, P60 DK-20541, P60 DK020541, R01 DK-45024, R01 DK045024] Funding Source: Medline
- NIGMS NIH HHS [T32 GM007288, T32 GM-07288] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK045024, P60DK020541, R01DK048321, R01DK055758] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007288] Funding Source: NIH RePORTER
Ask authors/readers for more resources
The adipose-derived hormone resistin is postulated to link obesity to insulin resistance and diabetes. Here, the infusion of either resistin or the resistin-like molecule-beta (RELMbeta) rapidly induced severe hepatic but not peripheral insulin resistance. In the presence of physiologic hyperinsulinemia, the infusion of purified recombinant resistin, increasing circulating resistin levels by approximately twofold to 15-fold, inhibited glucose metabolism such that lower rates of glucose infusion were required to maintain the plasma glucose concentration at basal levels. The effects of resistin and RELMbeta on in vivo insulin action were completely accounted for by a marked increase in the rate of glucose production. These results support the notion that a novel family of fat- and gut-derived circulating proteins modulates hepatic insulin action.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available