Research
Hormonal
Intramyocellular triglyceride (IMTG) levels are not the direct cause of muscle insulin resistance; instead, active lipid intermediates like diacylglycerol (DAG) and ceramides are the likely culprits, explaining why insulin-sensitive athletes can have high IMTG.
High fat content in muscles (IMTG) does not automatically mean you are insulin resistant. The key is how that fat is broken down into active byproducts like DAG and ceramides. Exercise can increase IMTG while improving insulin sensitivity by promoting healthy lipid partitioning.
GoodRefutesHIGH confidence
Such issues could be explained if the 'culprits' were active lipid moieties such as diacylglycerol and ceramide species, dependent more on lipid metabolism and partitioning than triglyceride amount.
Why this rating
Supported by multiple studies cited in the review, including comparisons of athletes vs. sedentary individuals.
Source
Adiposity and Insulin Resistance in Humans: The Role of the Different Tissue and Cellular Lipid Depots
Samantha Hocking et al. · Endocrine Reviews · 2013
DOI 10.1210/er.2012-1041
narrative_reviewCited 281×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Intra-abdominal (visceral) fat contributes to insulin resistance through mechanisms including high lipolytic activity, direct portal delivery of fatty acids to the liver, and secretion of inflammatory cytokines, whereas subcutaneous fat (particularly gluteofemoral) is metabolically protective.Good
- Hepatic lipid accumulation contributes to insulin resistance through the activation of protein kinase C (PKC) by diacylglycerols (DAGs), but liver lipid can also be a consequence of hyperinsulinemia stimulating lipid synthesis pathways.Good
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