Adiponectin treatment improves insulin resistance in mice by regulating the expression of the mitochondrial-derived peptide MOTS-c and its response to exercise via APPL1-SIRT1-PGC-1α.

Guo Q, Chang B, Yu QL, Xu ST, Yi XJ, Cao SC

Diabetologia3 Sept 2020Cited by 46 (Europe PMC)

PMID32880686DOI10.1007/s00125-020-05269-3PepBankPUB-32880686

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study8

1 result from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Mechanism
In mice, intraperitoneal MOTS‑c increased MOTS‑c levels and adiponectin mRNA and protein expression in plasma and skeletal muscle.
In plain wordsIn mice, injected MOTS‑c raised MOTS‑c levels and adiponectin expression in blood and muscle.
Peptide
MOTS-c
Outcome
IncreaseMOTS-c and adiponectin expression after MOTS-c injection
Study
mousen: not reported in source
High-fat-diet mice
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
Dose not stated · intraperitonealAs given in this study (mouse).
Source sentences
Summary
Exercise and i.p. Acrp30 or MOTS-c increased MOTS-c levels and adiponectin mRNA and protein expression in the plasma and skeletal muscle.
1 context sentence(design, population, supporting numbers)
Summary · context
To investigate this hypothesis, we used wild-type C57BL/6 mice subjected to high-fat diet, an exercise regimen, and i.p. injection of recombinant mouse adiponectin (Acrp30) or MOTS-c, and adiponectin knockout (Adipoq^-/-) mice (C57BL/6 background) subjected to i.p. injection of Acrp30.
Report a problemFND-3288068608

Natural levels measured7

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

02AnimalEndogenous levelAnimal study (in vivo)Mechanism
In adiponectin knockout mice, MOTS‑c levels in plasma and skeletal muscle were downregulated.
In plain wordsIn mice without adiponectin, the body's own MOTS‑c levels in blood and muscle were lower.
Peptide
MOTS-c
Outcome
DecreaseMOTS-c level in plasma and skeletal muscle
Study
mousen: not reported in source
Adiponectin knockout mice
Comparator
Wild-type mice
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
In Adipoq^-/- mice, MOTS-c levels in the plasma and skeletal muscle were downregulated.
1 context sentence(design, population, supporting numbers)
Summary · context
To investigate this hypothesis, we used wild-type C57BL/6 mice subjected to high-fat diet, an exercise regimen, and i.p. injection of recombinant mouse adiponectin (Acrp30) or MOTS-c, and adiponectin knockout (Adipoq^-/-) mice (C57BL/6 background) subjected to i.p. injection of Acrp30.
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-3288068601
03AnimalEndogenous levelAnimal study (in vivo)Mechanism
In mice, plasma and skeletal muscle MOTS‑c levels were significantly downregulated after a high-fat diet.
In plain wordsIn mice, a high-fat diet lowered the body's own MOTS‑c levels in blood and muscle.
Peptide
MOTS-c
Outcome
DecreaseMOTS-c level after high-fat diet
Study
mousen: not reported in source
High-fat-diet mice
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
In mice, plasma and skeletal muscle MOTS-c levels were significantly downregulated following high-fat-diet.
1 context sentence(design, population, supporting numbers)
Summary · context
To investigate this hypothesis, we used wild-type C57BL/6 mice subjected to high-fat diet, an exercise regimen, and i.p. injection of recombinant mouse adiponectin (Acrp30) or MOTS-c, and adiponectin knockout (Adipoq^-/-) mice (C57BL/6 background) subjected to i.p. injection of Acrp30.
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-3288068606
04AnimalEndogenous levelAnimal study (in vivo)Mechanism
In mice, exercise and intraperitoneal Acrp30 increased MOTS‑c levels in plasma and skeletal muscle.
In plain wordsIn mice, exercise and adiponectin injection raised the body's own MOTS‑c levels in blood and muscle.
Peptide
MOTS-c
Outcome
IncreaseMOTS-c level after exercise or Acrp30
Study
mousen: not reported in source
Mice with exercise or Acrp30 injection
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
Exercise and i.p. Acrp30 or MOTS-c increased MOTS-c levels and adiponectin mRNA and protein expression in the plasma and skeletal muscle.
1 context sentence(design, population, supporting numbers)
Summary · context
To investigate this hypothesis, we used wild-type C57BL/6 mice subjected to high-fat diet, an exercise regimen, and i.p. injection of recombinant mouse adiponectin (Acrp30) or MOTS-c, and adiponectin knockout (Adipoq^-/-) mice (C57BL/6 background) subjected to i.p. injection of Acrp30.
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-3288068607
05LabEndogenous levelIn vitro (cells)Mechanism
In C2C12 myotubes, adiponectin increased the mRNA expression of MOTS‑c.
In plain wordsIn cells, adiponectin raised the body's own MOTS‑c gene activity.
Peptide
MOTS-c
Outcome
IncreaseMOTS-c mRNA expression after adiponectin
Study
mousen: not reported in source
C2C12 myotubes
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
In C2C12 myotubes, adiponectin increased the mRNA expression of MOTS-c.
1 context sentence(design, population, supporting numbers)
Summary · context
C2C12 myotubes were also treated with sirtuin 1 (SIRT1) inhibitor, PGC-1α inhibitor, SIRT1 activator, plasmid-expressed active APPL1 (adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper), pcDNA-SIRT1, or siRNA against APPL1, SIRT1 or PGC-1α.
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-3288068602
06LabEndogenous levelIn vitro (cells)Mechanism
In C2C12 myotubes, APPL1 protein level after adiponectin treatment correlated positively with MOTS‑c protein and mRNA levels.
In plain wordsIn cells, more APPL1 after adiponectin went with more of the body's own MOTS‑c.
Peptide
MOTS-c
Outcome
IncreaseCorrelation of APPL1 with MOTS-c protein and mRNA
Study
mousen: not reported in source
C2C12 myotubes
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
APPL1 protein level following adiponectin treatment positively correlated with MOTS-c protein and mRNA levels in C2C12 myotubes.
1 context sentence(design, population, supporting numbers)
Summary · context
C2C12 myotubes were also treated with sirtuin 1 (SIRT1) inhibitor, PGC-1α inhibitor, SIRT1 activator, plasmid-expressed active APPL1 (adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper), pcDNA-SIRT1, or siRNA against APPL1, SIRT1 or PGC-1α.
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-3288068603
07LabEndogenous levelIn vitro (cells)Mechanism
In C2C12 myotubes, SIRT1 overexpression increased the adiponectin-induced mRNA and protein expression of MOTS‑c, SIRT1 and PGC-1α.
In plain wordsIn cells, extra SIRT1 raised the body's own MOTS‑c made after adiponectin treatment.
Peptide
MOTS-c
Outcome
IncreaseAdiponectin-induced MOTS-c expression with SIRT1 overexpression
Study
mousen: not reported in source
C2C12 myotubes
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
SIRT1 overexpression increased the adiponectin-induced mRNA and protein expression of MOTS-c, SIRT1 and PGC-1α.
1 context sentence(design, population, supporting numbers)
Summary · context
C2C12 myotubes were also treated with sirtuin 1 (SIRT1) inhibitor, PGC-1α inhibitor, SIRT1 activator, plasmid-expressed active APPL1 (adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper), pcDNA-SIRT1, or siRNA against APPL1, SIRT1 or PGC-1α.
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-3288068604
08LabEndogenous levelIn vitro (cells)Mechanism
In C2C12 myotubes, pharmacologic and genetic inhibition of PGC-1α suppressed the SIRT1-induced increases in MOTS‑c mRNA and protein.
In plain wordsIn cells, blocking PGC-1α stopped the rise in the body's own MOTS‑c caused by extra SIRT1.
Peptide
MOTS-c
Outcome
DecreaseMOTS-c expression after PGC-1α inhibition
Study
mousen: not reported in source
C2C12 myotubes
Outcome group
Receptor activity and mechanism · Metabolic and weight
Source sentences
Summary
Pharmacologic and genetic inhibition of PGC-1α suppressed the increases in MOTS-c mRNA and protein levels induced by SIRT1 overexpression.
1 context sentence(design, population, supporting numbers)
Summary · context
C2C12 myotubes were also treated with sirtuin 1 (SIRT1) inhibitor, PGC-1α inhibitor, SIRT1 activator, plasmid-expressed active APPL1 (adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper), pcDNA-SIRT1, or siRNA against APPL1, SIRT1 or PGC-1α.
This result measures the body's own MOTS-c. Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-3288068605

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
9 Oct 2026, 18:17 UTC
Study results updated
Version 1
9 Oct 2026, 02:47 UTC
First added · source update from Europe PMC

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Terms as the source lists them.

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Keywords

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