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Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of type 2 diabetic parents
Open accessAbstract
To further explore the nature of the mitochondrial dysfunction and insulin resistance that occur in the muscle of young, lean, normoglycemic, insulin-resistant offspring of parents with type 2 diabetes (IR offspring), we measured mitochondrial content by electron microscopy and insulin signaling in muscle biopsy samples obtained from these individuals before and during a hyperinsulinemic-euglycemic clamp. The rate of insulin-stimulated muscle glucose uptake was approximately 60% lower in the IR offspring than the control subjects and was associated with an approximately 60% increase in the intramyocellular lipid content as assessed by H magnetic resonance spectroscopy. Muscle mitochondrial density was 38% lower in the IR offspring. These changes were associated with a 50% increase in IRS-1 Ser312 and IRS-1 Ser636 phosphorylation and an approximately 60% reduction in insulin-stimulated Akt activation in the IR offspring. These data provide new insights into the earliest defects that may be responsible for the development of type 2 diabetes and support the hypothesis that reductions in mitochondrial content result in decreased mitochondrial function, which predisposes IR offspring to intramyocellular lipid accumulation, which in turn activates a serine kinase cascade that leads to defects in insulin signaling and action in muscle.
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“Moreover, alterations in muscle PGC-1␣ and - mRNA expression are observed in humans with insulin resistance-being reduced by nearly 50% in muscle from individuals with diabetes (122, 145) and in some populations of normoglycemic insulin-resistant humans (121, 124, 137).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [124]
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In the citing paper
“Increased serine phosphorylation of IRS-1 has been shown to impair insulin signaling (tyrosine phosphorylation of both insulin resistance and IRS-1) in type 2 diabetes ( 56 ).”
From Skeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes (2009) · cites this paper as [56]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Whereas mitochondria from NGT subjects without any family history of diabetes responded to insulin by increasing ATP production by 90%, mitochondria from insulin-resistant offspring increased ATP production by only 5% (Fig. A13).”
From Skeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes (2009) · cites this paper as [57]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“A number of physiological aspects of aging are also found in obesity and diabetes (Fig. 2) including accumulation of ectopic lipids and lipotoxicity in metabolic organs such as liver, skeletal muscle and heart, as well as decreased mitochondrial number and activity [144–147].”
From Targeting Intramyocellular Lipids to Improve Aging Muscle Function (2025) · cites this paper as [146]
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In the citing paper
“In lean insulin-resistant NGT offspring of type 2 diabetic parents, increased serine phosphorylation of IRS-1 in skeletal muscle has been documented in association with impaired activation of Akt ( 57 ) (Fig. A11).”
From Skeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes (2009) · cites this paper as [57]
In the citing paper
“Mitochondrial mass is consistently 14–38% lower in muscle in obesity and type 2 diabetes (2–5).”
In the citing paper
“Electron microscopic studies have revealed a significant reduction (~40%) in mitochondrial density in skeletal muscle in lean NGT offspring of type 2 diabetic parents, in obese nondiabetic individuals and in T2DM subjects compared to lean insulin-sensitive, age-matched controls [111, 112].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [111]
In the citing paper
“Rodent and human studies have suggested increased serine phosphorylation of IRS-1 in insulin resistant states [111, 171–173].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [111]
In the citing paper
“Additional studies confirmed that mitochondrial content is decreased and many factors regulating mitochondria are altered in obese, insulin-resistant adults as well as the offspring of parents with T2D (33,(78)(79)(80)(81)(82).”
From Altered mitochondrial function in insulin-deficient and insulin-resistant states (2018) · cites this paper as [79]
In the citing paper
“Thus, at least in this cohort, a reduction in mitochondrial content probably accounted for the reduced rate of oxidative phosphorylation in mitochondria.”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [44]
In the citing paper
“Importantly, similar reductions in OXPHOS gene expression have been observed in some, but not all, populations of insulin-resistant, but completely normoglycemic, individuals (122, 124).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [124]
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Amino Acid Supplements and Diabetes
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Metadata
- Authors
- Morino, K.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Morino, K.
- ORCID
- Morino, K.
- Venue
- Journal of Clinical Investigation
- Published
- 2005-12-01
- Volume
- 115
- Issue
- 12
- Pages
- 3587-3593
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1280967
- OpenAlex
- W2136942127
- Cited by
- 811
- References
- 40
- Citations by year
- 2026: 6 · 2025: 18 · 2024: 22 · 2023: 32 · 2022: 33 · 2021: 22 · 2020: 41 · 2019: 20 · 2018: 42 · 2017: 40 · 2016: 30 · 2015: 41 · 2014: 50 · 2013: 61 · 2012: 61
- FWCI
- 15.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association (DK-49230)
- National Institutes of Health (P30 DK, RR-00125, DK-45735)
- National Institute on Aging (R01AG023686)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK063192, R01DK049230, R01DK040936, P30DK045735, P01DK068229)
- National Center for Research Resources (M01RR000125)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- insulin resistance, type 2 diabetes, offspring of diabetic parents, mitochondrial density, mitochondrial dysfunction, IRS-1 serine phosphorylation, insulin signaling, Akt activation, intramyocellular lipid, muscle glucose uptake, hyperinsulinemic-euglycemic clamp, genetic susceptibility to diabetes
- MeSH terms
- Biopsy, Blood Glucose, Body Weight, Diabetes Mellitus, Type 2, DNA, Mitochondrial, Family Health, Female, Gene Expression Regulation, Glucose Tolerance Test, Humans, Hyperinsulinism, Insulin, Insulin Resistance, Lipids, Male, Microscopy, Electron, Mitochondria, Muscles, Phosphoproteins, Phosphorylation, RNA, Messenger, Serine, Time Factors, Transcription, Genetic, Triglycerides, Blotting, Western, Glucose Clamp Technique, Signal Transduction, Body Mass Index, Protein Serine-Threonine Kinases, Reverse Transcriptase Polymerase Chain Reaction, Microscopy, Electron, Transmission, Immunoprecipitation, Insulin Receptor Substrate Proteins
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