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Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Cell+Metab 2017 ; 26 (1): 157-170.e7 Nephropedia Template TP
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Inhibition of IKK? and TBK1 improves glucose control in a subset of patients with type 2 diabetes #MMPMID28683283
Oral EA; Reilly SM; Gomez AV; Meral R; Butz L; Ajluni N; Chenevert TL; Korytnaya E; Neidert A; Hench R; Rus D; Horowitz J; Poirier B; Zhao P; Lehmann K; Jain M; Yu R; Liddle C; Ahmadian M; Downes M; Evans RM; Saltiel AR
Cell Metab 2017[Jul]; 26 (1): 157-170.e7 PMID28683283show ga
Numerous studies indicate an inflammatory link between obesity and type 2 diabetes. The inflammatory kinases IKK? and TBK1 are elevated in obesity; their inhibition in obese mice reduces weight, insulin resistance, fatty liver and inflammation. Here we studied amlexanox, an inhibitor of IKK?/TBK1, in a proof-of-concept randomized, double blind, placebo-controlled study of 42 obese patients with type 2 diabetes and nonalcoholic fatty liver disease. Treatment of patients with amlexanox produced a statistically significant reduction in Hemoglobin A1c and fructosamine. Interestingly, a subset of drug responders also exhibited improvements in insulin sensitivity and hepatic steatosis. This subgroup was characterized by a distinct inflammatory gene expression signature from biopsied subcutaneous fat at baseline. They also exhibited a unique pattern of gene expression changes in response to amlexanox, consistent with increased energy expenditure. Together, these data suggest that IKK?/TBK1 inhibitors may be effective therapies for metabolic disease in an identifiable subset of patients.