Cited by 71Regulation of Appetite and ObesityMetabolism, Diabetes, and CancerAdipokines, Inflammation, and Metabolic Diseases

Central leptin action improves skeletal muscle AKT, AMPK, and PGC1α activation by hypothalamic PI3K-dependent mechanism

Open access
Roman, Erika A.F.R., Reis, Daniel, Romanatto, Talita, Maimoni, Denis, Ferreira, Eduardo A., Santos, Gustavo A., Torsoni, Adriana S., Velloso, Licio A. +1 more·2010·Molecular and Cellular Endocrinology

Abstract

Central leptin action requires PI3K activity to modulate glucose homeostasis and peripheral metabolism. However, the mechanism behind this phenomenon is not clearly understood. We hypothesize that hypothalamic PI3K activity is important for the modulation of the AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) pathway, PGC1 alpha, and AKT in skeletal muscle (SM). To address this issue, we injected leptin into the lateral ventricle of rats. Hypothalamic JAK2 and AKT were activated by intracerebroventricular (ICV) injection of leptin in a time-dependent manner. Central leptin improved tolerance to glucose (GTT), increased PGC1 alpha expression, and AKT, AMPK, ACC and JAK2 phosphorylation in the soleus muscle. Previous ICV administration of either LY294002 or propranolol (IP) blocked these effects. We concluded that the activation of the hypothalamic PI3K pathway is important for leptin-induced AKT phosphorylation, as well as for active catabolic pathway through AMPK and PGC1 alpha in SM. Thus, a defective leptin signalling PI3K pathway in the hypothalamus may contribute to peripheral resistance to insulin associated to diet-induced obesity.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.mce.2009.08.007

Cites

63 of 63 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The mechanism of leptin action also appears to be related to increases in physiological malonyl-CoA in the arcuate nucleus, which promotes a reduction in food intake and body weight, using different mechanisms from those previously reported for ghrelin action, during energetically wealthy states.

    “The mechanism of leptin action also appears to be related to increases in physiological malonyl-CoA in the arcuate nucleus, which promotes a reduction in food intake and body weight, using different mechanisms to those previously reported for ghrelin action, during energetically wealthy states ([49](#B49), [141](#B141)).”

    From Mitochondrial fatty acid oxidation in obesity (2013) · cites this paper as [141]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

1 retracted

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Roman, E. A. F. R., Reis, D., Romanatto, T., Maimoni, D., Ferreira, E. A., Santos, G. A., Torsoni, A. S., Velloso, L. A., & Torsoni, M. A.
Affiliations
  • Universidade Estadual de Campinas (UNICAMP) (BR)
  • Universidade Braz Cubas (BR)
Venue
Molecular and Cellular Endocrinology
Publisher
Elsevier BV
Published
2010-01
Volume
314
Issue
1
Pages
62-69
ISSN
0303-7207 (ISSN-L)
OpenAlex
W1979220770
Cited by
71
References
62
Citations by year
2025: 3 · 2024: 1 · 2023: 1 · 2022: 6 · 2021: 4 · 2020: 4 · 2019: 2 · 2018: 3 · 2017: 3 · 2016: 9 · 2015: 5 · 2014: 7 · 2013: 8 · 2012: 6
FWCI
2.10
Type
journal article
Language
en
Open access
Locations
  • Molecular and Cellular Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Fundação de Amparo à Pesquisa do Estado de São Paulo
  • Conselho Nacional de Desenvolvimento Científico e Tecnológico
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
hypothalamus, PI3K signaling, Akt phosphorylation, AMPK, PGC-1α, acetyl-CoA carboxylase, skeletal muscle, glucose tolerance, insulin resistance, diet-induced obesity, JAK2, intracerebroventricular administration, LY294002, propranolol
MeSH terms
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Phosphoinositide-3 Kinase Inhibitors, Adrenergic beta-Antagonists, Animals, Chromones, Energy Metabolism, Glucose, Homeostasis, Hypothalamus, Insulin, Male, Morpholines, Propranolol, Transcription Factors, Signal Transduction, RNA-Binding Proteins, Rats, Wistar, Muscle, Skeletal, Phosphatidylinositol 3-Kinases, Leptin, Proto-Oncogene Proteins c-akt, Rats, Janus Kinase 2, AMP-Activated Protein Kinases

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review