Cited by 90Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismLipid metabolism and biosynthesis

Saturated fatty acids and insulin resistance

Open access
Funaki, Makoto·2009·The Journal of Medical Investigation

Abstract

Insulin resistance is one of the pathophysiological features of obesity and type 2 diabetes. Recent findings have linked insulin resistance to chronic low-grade inflammation in white adipose tissue. Excess storage of saturated fat in white adipose tissue due to a modern life style causes hypertrophy and hyperplasia of adipocytes, which exhibit attenuated insulin signaling due to their production and release of saturated fatty acids. These adipocytes recruit macrophages to white adipose tissue and, together with them, initiate a proinflammatory response. Proinflammatory factors and saturated fatty acids secreted into the bloodstream from white adipose tissue impair insulin signaling in non-adipose tissues, which causes whole-body insulin resistance.

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Crossref · 10.2152/jmi.56.88

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  • Chronic activation of proinflammatory signalling in skeletal muscle and adipose is a significant contributing factor in the development and progression of metabolic disorders such as insulin resistance, obesity and Type II diabetes.

    “There is mounting evidence that chronic activation of proinflammatory signalling in tissues such as skeletal muscle and adipose is a significant contributing factor in the development and progression of metabolic disorders such as insulin resistance, obesity and Type II diabetes [1, 2].”
  • The actions of proinflammatory stimuli impair control of numerous signalling pathways regulating skeletal muscle insulin signalling, glucose uptake, mitochondrial fuel oxidation and respiration, impacting negatively upon skeletal muscle energy homeostasis.

    “The actions of these stimuli serve to not only further induce tissue expression and secretion of IL-6 and TNFα (via the NFκB pathway, [3, 4]), but impair control of numerous signalling pathways regulating skeletal muscle insulin signalling, glucose uptake, mitochondrial fuel oxidation and respiration that impact negatively upon skeletal muscle energy homeostasis [2, 5–7].”

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Authors
Funaki, M.
Affiliations
Tokushima University Hospital (JP)
Corresponding author
Funaki, Makoto
Venue
The Journal of Medical Investigation
Published
2009
Volume
56
Issue
3,4
Pages
88-92
ISSN
  • 1343-1420 (ISSN-L)
  • 1349-6867
OpenAlex
W2127856503
Cited by
90
References
42
Citations by year
2026: 3 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 5 · 2021: 4 · 2020: 2 · 2019: 2 · 2018: 6 · 2017: 5 · 2016: 7 · 2015: 9 · 2014: 5 · 2013: 5 · 2012: 9
FWCI
0.97
Type
journal article
Language
en
Open access
Locations
  • The Journal of Medical Investigation (publishedVersion)
  • PubMed (publishedVersion)
  • Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords
saturated fatty acids, insulin resistance, white adipose tissue, low-grade inflammation, adipocyte hypertrophy, adipocyte hyperplasia, macrophage recruitment, pro-inflammatory response, insulin signaling, obesity, type 2 diabetes
MeSH terms
Endocrine System, Energy Metabolism, Fatty Acids, Humans, Inflammation, Insulin Resistance, Macrophages, Obesity, Signal Transduction, Adipose Tissue, White

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