Mitohormesis in Hypothalamic POMC Neurons Mediates Regular Exercise-Induced High-Turnover Metabolism

Kang, Gil Myoung; Min, Se Hee; Lee, Chan Hee; Kim, Jee Ye; Lim, Hyunseob; Choi, Min Jeong; Jung, Saet Byel; Park, Jae-Woo; Kim, Seong-Jun; Park, Chae Beom; Dugu, Hong; Choi, Jong Han; Jang, Won Hee; Park, Se Eun; Cho, Young Min; Kim, Jae Geun; Kim, Kyung Gon; Choi, Cheol Soo; Kim, Young–Bum; Lee, Changhan; Shong, Minho; Kim, Min Seon

doi:10.1016/j.cmet.2021.01.003

Cited by 57 publications

(51 citation statements)

References 67 publications

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“…Further research found that the level of Pomc transcription is upregulated by mitochondrial DNA-encoded peptide (MOTS-c) in coordination with STAT3. β-Endorphin, which potentially plays an indispensable role in mediating the communication between POMC neurons and distant adipose tissues, is markedly induced by CRIF1 heterodeficiency ( 99 ). This explains the controversial role of CRIF1 played before.…”

Section: Crif1 In Mitochondria-related Diseasesmentioning

confidence: 99%

Multifunctions of CRIF1 in cancers and mitochondrial dysfunction

Jiang

Xiang²,

Lin³

et al. 2022

Front. Oncol.

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Sustaining proliferative signaling and enabling replicative immortality are two important hallmarks of cancer. The complex of cyclin-dependent kinase (CDK) and its cyclin plays a decisive role in the transformation of the cell cycle and is also critical in the initiation and progression of cancer. CRIF1, a multifunctional factor, plays a pivotal role in a series of cell biological progresses such as cell cycle, cell proliferation, and energy metabolism. CRIF1 is best known as a negative regulator of the cell cycle, on account of directly binding to Gadd45 family proteins or CDK2. In addition, CRIF1 acts as a regulator of several transcription factors such as Nur77 and STAT3 and partly determines the proliferation of cancer cells. Many studies showed that the expression of CRIF1 is significantly altered in cancers and potentially regarded as a tumor suppressor. This suggests that targeting CRIF1 would enhance the selectivity and sensitivity of cancer treatment. Moreover, CRIF1 might be an indispensable part of mitoribosome and is involved in the regulation of OXPHOS capacity. Further, CRIF1 is thought to be a novel target for the underlying mechanism of diseases with mitochondrial dysfunctions. In summary, this review would conclude the latest aspects of studies about CRIF1 in cancers and mitochondria-related diseases, shed new light on targeted therapy, and provide a more comprehensive holistic view.

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Section: Crif1 In Mitochondria-related Diseasesmentioning

confidence: 99%

Multifunctions of CRIF1 in cancers and mitochondrial dysfunction

Jiang

Xiang²,

Lin³

et al. 2022

Front. Oncol.

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“…Systemic coordination of the mitochondrial stress response is also conserved in mammals. In mice, mitochondrial dysfunction in the hypothalamic POMC neurons leads to high-turnover metabolism and obesity and remodels adipose metabolism [111,112]. Patients with mitochondrial disorders who suffer from muscle weakness have excessive levels of fibroblast growth factor 21 (FGF-21) and growth differentiation factor 15 (GDF-15) in their serum [113,114].…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial-to-nuclear communication in aging: an epigenetic perspective

Zhu

Tian

2022

Trends in Biochemical Sciences

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“…Hypothalamic gene expression was analyzed in mice administered OLZ or OLZ + MET for 5 days. The method for isolating the mediobasal hypothalamus was based on the previous studies ( Kim et al, 2006 ; Han et al, 2014 ; Lee et al, 2018 ; Kang et al, 2021 ). Briefly, mice with ad libitum access to food were sacrificed by decapitation.…”

Section: Methodsmentioning

confidence: 99%

Metformin ameliorates olanzapine-induced obesity and glucose intolerance by regulating hypothalamic inflammation and microglial activation in female mice

Suh

Lee²,

Kim³

et al. 2022

Front. Pharmacol.

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Olanzapine (OLZ), a widely used second-generation antipsychotic drug, is known to cause metabolic side effects, including diabetes and obesity. Interestingly, OLZ-induced metabolic side effects have been demonstrated to be more profound in females in human studies and animal models. Metformin (MET) is often used as a medication for the metabolic side effects of OLZ. However, the mechanisms underlying OLZ-induced metabolic disturbances and their treatment remain unclear. Recent evidence has suggested that hypothalamic inflammation is a key component of the pathophysiology of metabolic disorders. On this background, we conducted this study with the following three objectives: 1) to investigate whether OLZ can independently induce hypothalamic microgliosis; 2) to examine whether there are sex-dependent differences in OLZ-induced hypothalamic microgliosis; and 3) to examine whether MET affects hypothalamic microgliosis. We found that administration of OLZ for 5 days induced systemic glucose intolerance and hypothalamic microgliosis and inflammation. Of note, both hypothalamic microglial activation and systemic glucose intolerance were far more evident in female mice than in male mice. The administration of MET attenuated hypothalamic microglial activation and prevented OLZ-induced systemic glucose intolerance and hypothalamic leptin resistance. Minocycline, a tetracycline derivative that prevents microgliosis, showed similar results when centrally injected. Our findings reveal that OLZ induces metabolic disorders by causing hypothalamic inflammation and that this inflammation is alleviated by MET administration.

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Mitohormesis in Hypothalamic POMC Neurons Mediates Regular Exercise-Induced High-Turnover Metabolism

Cited by 57 publications

References 67 publications

Multifunctions of CRIF1 in cancers and mitochondrial dysfunction

Multifunctions of CRIF1 in cancers and mitochondrial dysfunction

Mitochondrial-to-nuclear communication in aging: an epigenetic perspective

Metformin ameliorates olanzapine-induced obesity and glucose intolerance by regulating hypothalamic inflammation and microglial activation in female mice

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