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EXENATIDE LEADS TO REDUCTION IN LIVER ENZYMES IN DIABETICS INDEPENDENT OF WEIGHT LOSS

May 20, 2008
 

I just got back from the AACE Annual sessions in Orlando. It was great to see a lot of you and appreciated the nice comments you had about our newsletter. I did not have a lot of time to put together an overview for out deadline but did want to share an abstract of interest. Deepti Bulchandani, MD and his colleagues have looked at Exenatide for the treatment of elevated enzymes in Non alcoholic fatty liver disease. This is another possible reason to start your patients on Exenatide. Click here to learn more.

EXENATIDE LEADS TO REDUCTION IN LIVER ENZYMES IN DIABETICS INDEPENDENT OF WEIGHT LOSS

Deepti Bulchandani, MD, Jagdish S Nachnani, MD, Crystal Eaton, LPN, and Mitchell Hamburg, MD, FACE

Objective:
Exenatide is a peptide receptor of the GLP-1(Glucagon like peptide 1) receptor which promotes insu­lin secretion. Raised liver enzymes in diabetics has been postulated to be due to Non alcoholic fatty liver disease (NAFLD) which is one of the commonest liver diseases and has been associated with Type 2 diabetes mellitus(DM) and insulin resistance. Exenatide has been shown to reverse hepatic steatosis in the animal model of fatty liver. However, there have been no studies looking at the asso­ciation of liver enzymes with the use of exenatide.

Methods:
From January 2007 till date, 29 eligible patients who had completed exetanide for a period of one year were included in our study. The patients were continu­ing their sulfonylurea/metformin treatment per their treat­ing endocrinologist. Demographic, anthropometric and laboratory were retrospectively collected. Paired t test and Pearson’s correlation coefficient was used for comparison.A two tailed p value of 0.05 was considered statistically significant.

Results:
There were 29 patients in our study cohort. The mean age (+/- standard deviation) of the patients was 55.5(8.1) years. 59% of the patients were males. The mean weight, HgBA1C, AST and ALT was 239 +/- 51 lbs, 8.2 +/- 1.3%, 31.3 +/- 15.6 units/L and 37.5 +/- 16.0 units/L respectively prior to starting exetanide therapy. 12/29 patients had either AST or ALT > 35 units/L. The mean decrease in weight at one year was 10. 8 lbs (p=0.005) and the mean decrease in HgBA1C was 0.7(p=0.001). The mean decrease at one year in AST was 6.5 units/L (p=0.04) and ALT was 11.9 units/L (p=0.001) respectively. There was no correlation with reduction in AST(p=0.51) or ALT(p=0.50)with change in weight. Out of the 12 patients with raised liver enzymes, in 7 patients the liver enzymes returned back to normal.

Discussion:
NAFLD has emerged as the most com­mon chronic liver disease in United States. Diabetes has been implicated as a risk factor in NAFLD. In fact the commonest reason for aymptomatic raised liver enzymes in diabetics has been postulated to be NAFLD. In our study exetanide has been shown to reduce liver enzymes after one year of treatment. It may possible that this could be an independent effect of exetanide or it could be secondary to the loss of weight accompanied with the use of exetanide. However, it our study, change in weight did not seem to be correlated with the reduction in liver enzymes and the effect was probably secondary to the use of exetanide.

Conclusions:
In patients with Type 2 DM, exetanide treatment leads to decrease in AST and ALT along with a mean reduction of weight and HgBA1C. It is possible that exetanide may be a possible therapy option in NAFLD in patients with raised liver function tests though fur­ther prospective studies will be needed to delineate that association.

Abstracts of the 17th Annual Meeting and Clinical Congress of the AACE