Lipid accumulation in non-adipose tissue and lipotoxicity
Open accessAbstract
Obesity is a well-known risk factor for the development of type 2 diabetes mellitus and cardiovascular disease. Importantly, obesity is not only associated with lipid accumulation in adipose tissue, but also in non-adipose tissues. The latter is also known as ectopic lipid accumulation and may be a possible link between obesity and its comorbidities such as insulin resistance, type 2 diabetes mellitus and cardiovascular disease. In skeletal muscle and liver, lipid accumulation has been associated with the development of insulin resistance, an early hallmark of developing type 2 diabetes mellitus. More specifically, accumulation of intermediates of lipid metabolism, such as diacylglycerol (DAG) and Acyl-CoA have been shown to interfere with insulin signaling in these tissues. Initially, muscular and hepatic insulin resistance can be overcome by an increased insulin production by the pancreas, resulting in hyperinsulinemia. However, during the progression towards overt type 2 diabetes, pancreatic failure occurs resulting in reduced insulin production. Interestingly, also in the pancreas lipid accumulation has been shown to precede dysfunction. Finally, accumulation of fat in the heart has been associated with cardiac dysfunction and heart failure, which may be an explanation for diabetic cardiomyopathy. Taken together, we conclude that evidence for deleterious effects of lipid accumulation in non-adipose tissue (lipotoxicity) is strong. However, while ample human data is available for skeletal muscle and the liver, future research should focus on lipid accumulation in the pancreas and the heart.
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Cellular and animal experiments suggest that signaling lipids other than triglyceride, such as ceramides or diacylglycerols, may be pathological.
“Cellular and animal experiments suggest that signaling lipids other than triglyceride, such as ceramides or diacylglycerols, may be pathological (131).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [131]
BMI is not the best method to determine obesity in the elderly because aging changes body composition, affecting BMI cut-off points.
“Furthermore, BMI is not the best method to determine obesity in the elderly because there are changes in the body composition during aging (body fat redistribution and muscle mass and bone density reductions), affecting the cut-off points for BMI [8, 34, 40].”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [34]
Decreased insulin secretion by the pancreas is derived from elevated concentrations of fatty acids, which induce β-cell apoptosis and reduce proliferation of pancreatic cells.
“Together with these events, the decreased insulin secretion by the pancreas is derived from elevated concentrations of fatty acids, which induces β-cell apoptosis and reduces proliferation of pancreatic cells [14, 16, 34–36].”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [34]
The mechanism of myosteatosis-induced insulin resistance involves impaired insulin signaling by lipidic intermediates such as diacylglycerol, long-chain acyl-coenzyme A, and ceramide, which inhibit GLUT-4 translocation to the sarcolemma.
“The mechanism involves the impaired insulin signaling by interacting with lipidic intermediates such as diacylglycerol (DAG), long-chain acyl-coenzyme A, and ceramide. These interactions at various levels inhibit the GLUT-4 translocation to the sarcolemma.”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [34]
Pathological myosteatosis in aging and obesity is associated with decreased insulin sensitivity and muscle mass and strength loss.
“Pathological myosteatosis in aging and obesity is associated with decreased insulin sensitivity and muscle mass and strength loss.”
From The critical role of oxidative stress in sarcopenic obesity (2021) · cites this paper as [34]
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- Authors
- van Herpen, N. A., & Schrauwen-Hinderling, V. B.
- Venue
- Physiology & Behavior
- Publisher
- Elsevier BV
- Published
- 2008-05
- Volume
- 94
- Issue
- 2
- Pages
- 231-241
- ISSN
- 0031-9384 (ISSN-L)
- OpenAlex
- W1989824965
- Cited by
- 500
- References
- 128
- Citations by year
- 2026: 14 · 2025: 19 · 2024: 22 · 2023: 25 · 2022: 33 · 2021: 38 · 2020: 32 · 2019: 26 · 2018: 33 · 2017: 25 · 2016: 28 · 2015: 34 · 2014: 34 · 2013: 29 · 2012: 28
- FWCI
- 10.96
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Physiology & Behavior (publishedVersion)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Keywords
- ectopic fat deposition, lipotoxicity, obesity, type 2 diabetes, insulin resistance, skeletal muscle, liver, diacylglycerol, acyl-CoA, hyperinsulinemia, beta-cell dysfunction, myocardial lipid accumulation, diabetic cardiomyopathy, cardiovascular disease
- MeSH terms
- Animals, Humans, Lipids, Liver, Myocardium, Obesity, Pancreas, Muscle, Skeletal, Lipid Metabolism
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