Advances in Adiponectin

Topic Information

Dear Colleagues,

Adiponectin, an adipokine secreted predominantly by adipose tissue, has garnered significant interest in recent years for its myriad beneficial roles in metabolic processes. Adiponectin operates via interaction with two primary receptors, AdipoR1 and AdipoR2, signaling primarily through Adenosine Monophosphate-Activated Protein Kinase (AMPK) and Peroxisome Proliferator-Activated Receptor-α (PPAR-α) pathways. A plethora of studies underscored the inverse correlation between adiponectin levels and incidences of metabolic syndromes, including obesity and type 2 diabetes. Adiponectin exhibits insulin-sensitizing properties by increasing glucose uptake, suppressing hepatic glucose output, and boosting fatty acid oxidation. It also exerts anti-inflammatory and anti-atherogenic effects, thereby providing cardiovascular protection. Recent advancements revealed that hypoadiponectinemia is implicated in several pathologies, from insulin resistance to cardio-cerebrovascular diseases and various types of cancer, signifying its diagnostic and prognostic potential. Moreover, adiponectin treatment or interventions elevating circulatory adiponectin levels may present therapeutic modalities to counteract these disorders. The regulation of adiponectin and its receptors is multifaceted, involving intricate genetic, epigenetic, transcriptional, and post-translational processes. Unraveling the complexities of these regulatory mechanisms can help explain adiponectin’s role in health and disease. Furthermore, the exploration of adiponectin's association with other hormones and metabolic pathways is propelling the research field toward a more comprehensive understanding of endocrine and metabolic regulation. In particular, studies are beginning to unravel adiponectin’s distinct roles in males and females, pointing towards sex-specific therapeutic approaches. Notwithstanding these advances, there remain challenging questions in the field. The molecular mechanisms underlying adiponectin’s seemingly contradictory roles in various tissues and conditions remain to be elucidated. Future investigations necessitate a deeper dive into the complexities of adiponectin signaling and its interplay with other metabolic pathways.

Prof. Dr. Puran S. Bora
Dr. Mayank Choubey
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomolecules biomolecules	4.8	9.4	2011	16.3 Days	CHF 2700	Submit
Cancers cancers	4.5	8.0	2009	16.3 Days	CHF 2900	Submit
International Journal of Molecular Sciences ijms	4.9	8.1	2000	18.1 Days	CHF 2900	Submit
Nutrients nutrients	4.8	9.2	2009	17.5 Days	CHF 2900	Submit
Antioxidants antioxidants	6.0	10.6	2012	15.5 Days	CHF 2900	Submit

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Published Papers (3 papers)

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17 pages, 2438 KiB  

Open AccessArticle

Striking Cardioprotective Effects of an Adiponectin Receptor Agonist in an Aged Mouse Model of Duchenne Muscular Dystrophy

by Michel Abou-Samra, Nicolas Dubuisson, Alice Marino, Camille M. Selvais, Versele Romain, Maria A. Davis-López de Carrizosa, Laurence Noel, Christophe Beauloye, Sonia M. Brichard and Sandrine Horman

Antioxidants 2024, 13(12), 1551; https://doi.org/10.3390/antiox13121551 - 18 Dec 2024

Viewed by 436

Abstract

Adiponectin (ApN) is a hormone with potent effects on various tissues. We previously demonstrated its ability to counteract Duchenne muscular dystrophy (DMD), a severe muscle disorder. However, its therapeutic use is limited. AdipoRon, an orally active ApN mimic, offers a promising alternative. While [...] Read more.

Adiponectin (ApN) is a hormone with potent effects on various tissues. We previously demonstrated its ability to counteract Duchenne muscular dystrophy (DMD), a severe muscle disorder. However, its therapeutic use is limited. AdipoRon, an orally active ApN mimic, offers a promising alternative. While cardiomyopathy is the primary cause of mortality in DMD, the effects of ApN or AdipoRon on dystrophic hearts have not been investigated. Our recent findings demonstrated the significant protective effects of AdipoRon on dystrophic skeletal muscle. In this study, we investigated whether AdipoRon effects could be extended to dystrophic hearts. As cardiomyopathy develops late in mdx mice (DMD mouse model), 14-month-old mdx mice were orally treated for two months with AdipoRon at a dose of 50 mg/kg/day and then compared with untreated mdx and wild-type (WT) controls. Echocardiography revealed cardiac dysfunction and ventricular hypertrophy in mdx mice, which were fully reversed in AdipoRon-treated mice. AdipoRon also reduced markers of cardiac inflammation, oxidative stress, hypertrophy, and fibrosis while enhancing mitochondrial biogenesis via ApN receptor-1 and CAMKK2/AMPK pathways. Remarkably, treated mice also showed improved skeletal muscle strength and endurance. By offering protection to both cardiac and skeletal muscles, AdipoRon holds potential as a comprehensive therapeutic strategy for better managing DMD. Full article

(This article belongs to the Topic Advances in Adiponectin)

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18 pages, 3700 KiB  

Open AccessArticle

Adiponectin Signaling Modulates Fat Taste Responsiveness in Mice

by Fangjun Lin, Emeline Masterson and Timothy A. Gilbertson

Nutrients 2024, 16(21), 3704; https://doi.org/10.3390/nu16213704 - 30 Oct 2024

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Abstract

Background/Objectives: Adiponectin, the most abundant peptide hormone secreted by adipocytes, is a well-known homeostatic factor regulating lipid metabolism and insulin sensitivity. It has been shown that the adiponectin receptor agonist AdipoRon selectively enhances cellular responses to fatty acids in human taste cells, and [...] Read more.

Background/Objectives: Adiponectin, the most abundant peptide hormone secreted by adipocytes, is a well-known homeostatic factor regulating lipid metabolism and insulin sensitivity. It has been shown that the adiponectin receptor agonist AdipoRon selectively enhances cellular responses to fatty acids in human taste cells, and adiponectin selectively increases taste behavioral responses to intralipid in mice. However, the molecular mechanism underlying the physiological effects of adiponectin on fat taste in mice remains unclear. Conclusions: Here we define AdipoR1 as the mediator responsible for the enhancement role of adiponectin/AdipoRon on fatty acid-induced responses in mouse taste bud cells. Methods and Results: Calcium imaging data demonstrate that AdipoRon enhances linoleic acid-induced calcium responses in a dose-dependent fashion in mouse taste cells isolated from circumvallate and fungiform papillae. Similar to human taste cells, the enhancement role of AdipoRon on fatty acid-induced responses was impaired by co-administration of an AMPK inhibitor (Compound C) or a CD36 inhibitor (SSO). Utilizing Adipor1-deficient animals, we determined that the enhancement role of AdipoRon/adiponectin is dependent on AdipoR1, since AdipoRon/adiponectin failed to increase fatty acid-induced calcium responses in taste bud cells isolated from these mice. Brief-access taste tests were performed to determine whether AdipoRon’s enhancement role was correlated with any differences in taste behavioral responses to fat. Although AdipoRon enhances the cellular responses of taste bud cells to fatty acids, it does not appear to alter fat taste behavior in mice. However, fat-naïve Adipor1^−/− animals were indifferent to increasing concentrations of intralipid, suggesting that adiponectin signaling may have profound effects on the ability of mice to detect fatty acids in the absence of previous exposure to fatty acids and fat-containing diets. Full article

(This article belongs to the Topic Advances in Adiponectin)

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20 pages, 29992 KiB  

Open AccessArticle

Challenging Sarcopenia: Exploring AdipoRon in Aging Skeletal Muscle as a Healthspan-Extending Shield

by Camille M. Selvais, Maria A. Davis-López de Carrizosa, Romain Versele, Nicolas Dubuisson, Laurence Noel, Sonia M. Brichard and Michel Abou-Samra

Antioxidants 2024, 13(9), 1073; https://doi.org/10.3390/antiox13091073 - 3 Sep 2024

Viewed by 1291

Abstract

Sarcopenia, characterized by loss of muscle mass, quality, and function, poses significant risks in aging. We previously demonstrated that long-term treatment with AdipoRon (AR), an adiponectin receptor agonist, alleviated myosteatosis and muscle degeneration in middle-aged obese mice. This study aimed to determine if [...] Read more.

Sarcopenia, characterized by loss of muscle mass, quality, and function, poses significant risks in aging. We previously demonstrated that long-term treatment with AdipoRon (AR), an adiponectin receptor agonist, alleviated myosteatosis and muscle degeneration in middle-aged obese mice. This study aimed to determine if a shorter AR treatment could effectively offset sarcopenia in older mice. Two groups of old mice (20–23 months) were studied, one untreated (O) and one orally-treated with AR (O-AR) at 50 mg/kg/day for three months, compared with control 3-month-old young mice (Y) or 10-month-old young-adult mice (C-10). Results showed that AR remarkably inversed the loss of muscle mass by restoring the sarcopenia index and fiber count, which were greatly diminished with age. Additionally, AR successfully saved muscle quality of O mice by halving the accumulation of tubular aggregates and aberrant mitochondria, through AMPK pathway activation and enhanced autophagy. AR also bolstered muscle function by rescuing mitochondrial activity and improving exercise endurance. Finally, AR markedly curbed muscle fibrosis and mitigated local/systemic inflammation. Thus, a late three-month AR treatment successfully opposed sarcopenia and counteracted various hallmarks of aging, suggesting AR as a promising anti-aging therapy for skeletal muscles, potentially extending healthspan. Full article

(This article belongs to the Topic Advances in Adiponectin)

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