Mitochondrial dynamics controlled by mitofusins regulate Agrp neuronal activity and diet-induced obesity

Dietrich, Marcelo O.; Liu, Zhong-Wu; Horvath, Tamas L.

doi:10.1016/j.cell.2013.09.004

Cited by 306Regulation of Appetite and ObesityMitochondrial Function and PathologyAdipose Tissue and Metabolism

Mitochondrial dynamics controlled by mitofusins regulate Agrp neuronal activity and diet-induced obesity

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Dietrich, Marcelo O., Liu, Zhong-Wu, Horvath, Tamas L.·2013·Cell

DOI 10.1016/j.cell.2013.09.004PMC PMC4142434

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Abstract

Mitochondria are key organelles in the maintenance of cellular energy metabolism and integrity. Here, we show that mitochondria number decrease but their size increase in orexigenic agouti-related protein (Agrp) neurons during the transition from fasted to fed to overfed state. These fusion-like dynamic changes were cell-type specific, as they occurred in the opposite direction in anorexigenic pro-opiomelanocortin (POMC) neurons. Interfering with mitochondrial fusion mechanisms in Agrp neurons by cell-selectively knocking down mitofusin 1 (Mfn1) or mitofusin 2 (Mfn2) resulted in altered mitochondria size and density in these cells. Deficiency in mitofusins impaired the electric activity of Agrp neurons during high-fat diet (HFD), an event reversed by cell-selective administration of ATP. Agrp-specific Mfn1 or Mfn2 knockout mice gained less weight when fed a HFD due to decreased fat mass. Overall, our data unmask an important role for mitochondrial dynamics governed by Mfn1 and Mfn2 in Agrp neurons in central regulation of whole-body energy metabolism.

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In mice, mitochondrial fusion increases in orexigenic NPY/Agrp neurons, inducing neuronal activity that controls storage of excess energy in fat when mice are fed a high-fat diet.
“In studies performed in mice it has been demonstrated that mitochondrial fusion increases in orexigenic NPY/Agrp neurons inducing neuronal activity that control the storage of excess of energy in fat when mice are fed with high-fat diet (Dietrich et al., 2013).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Dietrich et al., 2013
The activity of NPY/Agrp neurons is impaired when mitochondrial fusion mechanism is altered, producing resistance to fat gain during high-fat diet.
“The activity of these neurons is impaired when the mitochondrial fusion mechanism is altered producing resistance to fat gain during high fat diet (Dietrich et al., 2013).”
From Mitochondrial Activity and Dynamics Changes Regarding Metabolism in Ageing and Obesity (2017) · cites this paper as Dietrich et al., 2013
Defective mitochondrial dynamics and mitochondrial-ER communication in hypothalamic POMC and AgRP neurons might modify feeding behavior and whole-body energy homeostasis.
“Defective mitochondrial dynamics and mitochondrial-ER communication in hypothalamic POMC and AgRP neurons might actually modify feeding behavior and whole-body energy homeostasis (Dietrich et al, 2013; Schneeberger et al, 2013).”
From Mitochondrial response to nutrient availability and its role in metabolic disease (2014) · cites this paper as Dietrich et al, 2013

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Mitofusins: Mighty Regulators of Metabolism
Özcan, U. (2013) · Cell · doi:10.1016/j.cell.2013.09.013 · Cited by 14 · see citing works

Authors: Dietrich, M. O., Liu, Z.-W., & Horvath, T. L.
Affiliations: Universidade Federal do Rio Grande do Sul (BR)
Corresponding author: Dietrich, Marcelo O.
ORCID: Dietrich, Marcelo O.
Venue: Cell
Publisher: Elsevier BV
Published: 2013-09
Volume: 155
Issue: 1
Pages: 188-199
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2013.09.004
PMC: PMC4142434
OpenAlex: W1981102645
Cited by: 306
References: 60
Citations by year: 2026: 9 · 2025: 16 · 2024: 25 · 2023: 10 · 2022: 18 · 2021: 24 · 2020: 20 · 2019: 23 · 2018: 33 · 2017: 37 · 2016: 35 · 2015: 25 · 2014: 27 · 2013: 4
FWCI: 16.38
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 390 d)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Repository of the Academy's Library (Library of the Hungarian Academy of Sciences) (acceptedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute on Aging (R01AG040236)
National Institute of Diabetes and Digestive and Kidney Diseases (DP1DK098058, DP1 DK006850)
National Institute of Neurological Disorders and Stroke (P01NS062686)
Topics: Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords: mitochondrial dynamics, mitofusin 1, mitofusin 2, AgRP neurons, proopiomelanocortin neurons, diet-induced obesity, high-fat diet, mitochondrial fusion, neuronal electrical activity, ATP, energy metabolism, fat mass, orexigenic neurons, anorexigenic neurons
MeSH terms: Animals, Female, Male, Mitochondria, Neurons, Obesity, Sex Characteristics, Cell Death, Gene Deletion, GTP Phosphohydrolases, Mice, Organelle Shape, Organelle Size, Agouti-Related Protein, Gene Knockdown Techniques, Diet, High-Fat

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Mitochondrial dynamics controlled by mitofusins regulate Agrp neuronal activity and diet-induced obesity

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