Submitted on December 31, 2007
Accepted on September 23, 2008
Liver fat, visceral adiposity and sleep disturbances contribute to the development of insulin resistance and glucose intolerance in non diabetic dialysis patients
Giorgos K. Sakkas1*, Christina Karatzaferi2, Elias Zintzaras3, Christoforos D Giannaki1, Vassilios Liakopoulos1, Eleftherios Lavdas4, Eleni Damani5, Nikos Liakos6, Ioannis Fezoulidis4, Yiannis Koutedakis2, and Ioannis L Stefanidis1
1 Nephrology, University of Thessaly, Larissa, Greece
2 Sport Science, University of Thessaly, Trikala, Thessaly, Greece
3 Biomathematics, University of Thessaly, Larissa, Thessaly, Greece
4 Radiology, University of Thessaly, Larissa, Thessaly, Greece
5 Biochemistry, University of Thessaly, Larissa, Thessaly, Greece
6 Biochemistry, University of Thessaly, Greece
* To whom correspondence should be addressed. E-mail: gsakkas{at}med.uth.gr.
Hemodialysis (HD) patients exhibit insulin resistance (IR) in target organs such as liver, muscles and adipose tissue. The aim of the study was to indentify contributors to IR and to develop a model for predicting glucose intolerance in non-diabetic HD patients.
After an OGTT, 34 HD patients were divided in those with normal and those with impaired glucose tolerance. Indices of insulin sensitivity were calculated from OGTT data. Liver and muscle fat infiltration and central adiposity were measured by CT scans, body composition by DEXA, sleep quality by a full polysomnography, and functional capacity and quality of life were assessed by a battery of tests and questionnaires. Cut-off points, as well as sensitivity and specificity calculations were based on insulin resistance using a ROC curve analysis.
From 34 patients, 15 were found with impaired glucose tolerance test (IGT) while the rest composed the control group (NGT). Intrahepatic fat content and visceral adiposity were significantly increased in the IGT group. IR indices strongly correlated with sleep disturbances, visceral adiposity, functional capacity and quality of life. The oxygen desaturation during sleep, visceral adiposity, intrahepatic fat content and quality of life score were found to fit the model for predicting glucose intolerance.
Visceral and intrahepatic fat content, as well as quality of life and sleep seemed to be involved at some point in the development of glucose intolerance in HD patients. Means of reducing fat depots in the liver and splachnic area might be very helpful in combating the insulin resistance syndrome.
