Crosstalk between autophagy and insulin resistance: evidence from different tissues

Sadeghi, Asie; Niknam, Maryam; Momeni-Moghaddam, Mohammad Amin; Shabani, Maryam; Aria, Hamid; Bastin, Alireza; Teimouri, Maryam; Meshkani, Reza; Akbari, Hamed

doi:10.1186/s40001-023-01424-9

Cited by 18 publications

(3 citation statements)

References 308 publications

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“…The correlation between IR and PCOS has been so strongly represented that the drugs which increase insulin sensitization have been used as a treatment option for PCOS. Further, the mechanisms underlying IR are involved in energy imbalance and neuro-hormonal dysregulation, which are in turn regulated by autophagy (Purwar & Nagpure, 2022;Sadeghi et al, 2023;Zhao et al, 2023). The PCOS is affecting an ever-increasing number of women around the world and the role of autophagy therein, if properly understood, can be instrumental in treatment and management of the problem.…”

Section: Role Of Autophagy In Insulin Resistance Of Ovarian Cellmentioning

confidence: 99%

A review on the nexus of autophagy genes from the perspective of polycystic ovary syndrome

Khatun,

Nasrin,

Hassan

et al. 2024

Biology of the Cell

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Polycystic ovary syndrome or PCOS is an endocrine disorder in women of reproductive age. It is a diversified multi factorial disorder and diagnosis is very complicated because of its overlapping symptoms some of which are irregular menstrual cycle, acne in face, excess level of androgen (AE), insulin resistance, obesity, cardiovascular disease, mood disorder and type 2 diabetes (T2DM). PCOS may be caused by hormonal imbalance, genetic and epigenetic vulnerability, hypothalamic and ovarian troubles. PCOS is essentially hyperandrogenimia with oligo‐anovulation. This review explains the abnormal regulation of autophagy related genes and proteins in different cells at various stages which leads to the genesis of PCOS. During nutrient starvation cells face stress condition, which it tries to overcome by activating its macroautophagy mechanism and by degrading the cytoplasmic material. This provides energy to the cell facilitating its survival. Downregulation of autophagy related genes in endometria has been observed in PCOS women. PCOS can be managed by maintaining proper lifestyle and medical treatment. Healthy meals and regular exercise can prevent the excessive weight and also reduce the PCOS complications. Medicines such as metformin, clomiphene, and the oral contraceptive pill can also balance the hormonal level. The imbalance in regulation of autophagy genes has been discussed with correlation to PCOS. The different management strategies for PCOS have also been summarized.

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Section: Role Of Autophagy In Insulin Resistance Of Ovarian Cellmentioning

confidence: 99%

A review on the nexus of autophagy genes from the perspective of polycystic ovary syndrome

Khatun,

Nasrin,

Hassan

et al. 2024

Biology of the Cell

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“…In summary, the activation of JNK by IRE1 disrupts the signaling of the insulin receptor, leading to insulin resistance [225]. This process is facilitated by ER stress and inflammatory cytokines, both playing crucial roles [221].…”

Section: Er Stress and Insulin Signaling In Adipogenesismentioning

confidence: 99%

Endoplasmic Reticulum Stress and Its Impact on Adipogenesis: Molecular Mechanisms Implicated

Kim,

Lee,

et al. 2023

Nutrients

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Endoplasmic reticulum (ER) stress plays a pivotal role in adipogenesis, which encompasses the differentiation of adipocytes and lipid accumulation. Sustained ER stress has the potential to disrupt the signaling of the unfolded protein response (UPR), thereby influencing adipogenesis. This comprehensive review illuminates the molecular mechanisms that underpin the interplay between ER stress and adipogenesis. We delve into the dysregulation of UPR pathways, namely, IRE1-XBP1, PERK and ATF6 in relation to adipocyte differentiation, lipid metabolism, and tissue inflammation. Moreover, we scrutinize how ER stress impacts key adipogenic transcription factors such as proliferator-activated receptor γ (PPARγ) and CCAAT-enhancer-binding proteins (C/EBPs) along with their interaction with other signaling pathways. The cellular ramifications include alterations in lipid metabolism, dysregulation of adipokines, and aged adipose tissue inflammation. We also discuss the potential roles the molecular chaperones cyclophilin A and cyclophilin B play in adipogenesis. By shedding light on the intricate relationship between ER stress and adipogenesis, this review paves the way for devising innovative therapeutic interventions.

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“…Autophagy is commonly recognized as a defense mechanism able to promote either cell survival or cell death by adapting its machinery to different stimuli ( Sadeghi et al, 2023 ) including growth factors deficiencies, oxidative alterations, and metabolic changes. It is well known that autophagy is sensitive to nutrient status, and fluctuation in lipid level might serve as a physiological sensor for its regulation.…”

Section: Introductionmentioning

confidence: 99%

Autophagy and inflammation an intricate affair in the management of obesity and metabolic disorders: evidence for novel pharmacological strategies?

Friuli,

Sepe,

Panza

et al. 2024

Front. Pharmacol.

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Unhealthy lifestyle habits including a sedentary life, the lack of physical activity, and wrong dietary habits are the major ones responsible for the constant increase of obesity and metabolic disorders prevalence worldwide; therefore, the scientific community pays significant attention to the pharmacotherapy of such diseases, beyond lifestyle interventions, the use of medical devices, and surgical approaches. The intricate interplay between autophagy and inflammation appears crucial to orchestrate fundamental aspects of cellular and organismal responses to challenging stimuli, including metabolic insults; hence, when these two processes are dysregulated (enhanced or suppressed) they produce pathologic effects. The present review summarizes the existing literature reporting the intricate affair between autophagy and inflammation in the context of metabolic disorders, including obesity, diabetes, and liver metabolic diseases (non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH)). The evidence collected so far suggests that an alteration of autophagy might lead to maladaptive metabolic and inflammatory responses thus exacerbating the severity of the disease, and the most prominent conclusion underlies that autophagy might exert a protective function by contributing to balance inflammation. However, the complex nature of obesity and metabolic disorders might represent a limit of the studies; indeed, although many pharmacological treatments, producing positive metabolic effects, are also able to modulate autophagic flux and inflammation, it is not clear if the final beneficial effect might occur only by their mechanism of action, rather than because of additionally involved pathways. Finally, although future studies are needed, the observation that anti-obesity and antidiabetic drugs already on the market, including incretin mimetic agents, facilitate autophagy by dampening inflammation, strongly contributes to the idea that autophagy might represent a druggable system for the development of novel pharmacological tools that might represent an attractive strategy for the treatment of obesity and metabolic disorders.

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Crosstalk between autophagy and insulin resistance: evidence from different tissues

Cited by 18 publications

References 308 publications

A review on the nexus of autophagy genes from the perspective of polycystic ovary syndrome

A review on the nexus of autophagy genes from the perspective of polycystic ovary syndrome

Endoplasmic Reticulum Stress and Its Impact on Adipogenesis: Molecular Mechanisms Implicated

Autophagy and inflammation an intricate affair in the management of obesity and metabolic disorders: evidence for novel pharmacological strategies?

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