Alloveda Liver Update: Contribution of liver, kidney, and skeletal muscle in postprandial glucose homeostasis |
News and Updates
eMediNexus Coverage from: 
Alloveda Liver Update: Contribution of liver, kidney, and skeletal muscle in postprandial glucose homeostasis

0 Read Comments                

Plethora of evidence demonstrate the role for the kidney in postabsorptive glucose homeostasis. The current study was conducted to assess the role of the kidney in postprandial glucose homeostasis and to compare its influence to that of liver and skeletal muscle. The authors used the double isotope technique along with forearm and renal balance measurements to evaluate systemic, renal, and hepatic glucose release along with glucose uptake by kidney, skeletal muscle, and splanchnic tissues in 10 normal volunteers after ingestion of 75 g of glucose.

The outcome revealed that, during the 4.5-h postprandial period, 22 +/- 2 g, 30 +/- 3% of the ingested glucose was initially extracted by splanchnic tissues. 19 +/- 3 g (26 +/- 3% of the ingested glucose) out of the  53 +/- 2 g that entered the systemic circulation was availed by skeletal muscle while 7.5 +/- 1.7 g (10 +/- 2% of the ingested glucose) by the kidney. Endogenous glucose release during the postprandial period, measured as the difference between overall systemic glucose appearance and the appearance of ingested glucose in the systemic circulation was found to be suppressed 61 +/- 3%. However, renal glucose release got raised by twofold (10.6 +/- 2.5 g) that was reported for ~60% of postprandial endogenous glucose release. Hepatic glucose release (6.7 +/- 2.2 g), evaluated as the difference between endogenous and renal glucose release, was suppressed 82 +/- 6%.

Thus, based on these observations it can be concluded that previously unacknowledged, kidney has an impact on the postprandial glucose homeostasis, suggestive that postprandial suppression of hepatic glucose release is nearly twofold in contrast to that has been assessed as no renal glucose release in previous studies (42 +/- 4%). Therefore, it can be hypothesized that increase in postprandial renal glucose release is implicated in promoting effective liver glycogen repletion, mediated via substantial suppression of hepatic glucose release.

Source: Meyer C, Dostou JM, Welle SL, Gerich JE. Role of human liver, kidney, and skeletal muscle in postprandial glucose homeostasis. Am J Physiol Endocrinol Metab. 2002 Feb;282(2):E419-27. 

To comment on this article,
create a free account.
Sign Up to instantly read 30000+ free Articles & 1000+ Case Studies
Create Account

Already registered?

Login Now