Association of insulin resistance with the accumulation of saturated intramyocellular lipid: A comparison with other fat stores.
NMR in biomedicine 2024
Azhar M, Watson LPE, De Lucia Rolfe E, Ferraro M, Carr K, Worsley J, Boesch C, Hodson L, Chatterjee KK, Kemp GJ, Savage DB, Sleigh A
DOI : 10.1002/nbm.5117
PubMed ID : 38356104
PMCID :
URL : https://analyticalsciencejournals.onlinelibrary.wiley.com/doi/10.1002/nbm.5117
Abstract
It has been shown using proton magnetic resonance spectroscopy ( H MRS) that, in a group of females, whole-body insulin resistance was more closely related to accumulation of saturated intramyocellular lipid (IMCL) than to IMCL concentration alone. This has not been investigated in males. We investigated whether age- and body mass index-matched healthy males differ from the previously reported females in IMCL composition (measured as CH :CH ) and IMCL concentration (measured as CH ), and in their associations with insulin resistance. We ask whether saturated IMCL accumulation is more strongly associated with insulin resistance than other ectopic and adipose tissue lipid pools and remains a significant predictor when these other pools are taken into account. In this group of males, who had similar overall insulin sensitivity to the females, IMCL was similar between sexes. The males demonstrated similar and even stronger associations of IMCL with insulin resistance, supporting the idea that a marker reflecting the accumulation of saturated IMCL is more strongly associated with whole-body insulin resistance than IMCL concentration alone. However, this marker ceased to be a significant predictor of whole-body insulin resistance after consideration of other lipid pools, which implies that this measure carries no more information in practice than the other predictors we found, such as intrahepatic lipid and visceral adipose tissue. As the marker of saturated IMCL accumulation appears to be related to these two predictors and has a much smaller dynamic range, this finding does not rule out a role for it in the pathogenesis of insulin resistance.