Cardiac mitochondrial respiration following a low-carbohydrate, high-fat diet in apolipoprotein E-deficient mice

Rocha, Cynthia; Koury, Olivia Hanna; Scheede‐Bergdahl, Celena; Bergdahl, Andreas

doi:10.1007/s13105-018-0653-x

Cited by 4 publications

(2 citation statements)

References 34 publications

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“…Mitochondrial oxygen consumption, as determined by Seahorse respirometry, was also increased in pancreatic islets of HFD-fed mice. These results are also consistent with enhanced mitochondrial respiration or mitochondrial complex activity in cardiac or liver tissues of HFD-fed mice 89 , 90 . These mitochondrial changes could also be an adaptation to metabolic stress to meet the metabolic demand caused by obesity and insulin resistance.…”

Section: Functional Role Of Tfeb-mediated Mitophagy Under Conditions ...supporting

confidence: 84%

Pancreatic β-cell mitophagy as an adaptive response to metabolic stress and the underlying mechanism that involves lysosomal Ca2+ release

Oh,

Park,

Sonn

et al. 2023

Exp Mol Med

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Mitophagy is an excellent example of selective autophagy that eliminates damaged or dysfunctional mitochondria, and it is crucial for the maintenance of mitochondrial integrity and function. The critical roles of autophagy in pancreatic β-cell structure and function have been clearly shown. Furthermore, morphological abnormalities and decreased function of mitochondria have been observed in autophagy-deficient β-cells, suggesting the importance of β-cell mitophagy. However, the role of authentic mitophagy in β-cell function has not been clearly demonstrated, as mice with pancreatic β-cell-specific disruption of Parkin, one of the most important players in mitophagy, did not exhibit apparent abnormalities in β-cell function or glucose homeostasis. Instead, the role of mitophagy in pancreatic β-cells has been investigated using β-cell-specific Tfeb-knockout mice (TfebΔβ-cell mice); Tfeb is a master regulator of lysosomal biogenesis or autophagy gene expression and participates in mitophagy. TfebΔβ-cell mice were unable to adaptively increase mitophagy or mitochondrial complex activity in response to high-fat diet (HFD)-induced metabolic stress. Consequently, TfebΔβ-cell mice exhibited impaired β-cell responses and further exacerbated metabolic deterioration after HFD feeding. TFEB was activated by mitochondrial or metabolic stress-induced lysosomal Ca2+ release, which led to calcineurin activation and mitophagy. After lysosomal Ca2+ release, depleted lysosomal Ca2+ stores were replenished by ER Ca2+ through ER→lysosomal Ca2+ refilling, which supplemented the low lysosomal Ca2+ capacity. The importance of mitophagy in β-cell function was also demonstrated in mice that developed β-cell dysfunction and glucose intolerance after treatment with a calcineurin inhibitor that hampered TFEB activation and mitophagy.

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Section: Functional Role Of Tfeb-mediated Mitophagy Under Conditions ...supporting

confidence: 84%

Pancreatic β-cell mitophagy as an adaptive response to metabolic stress and the underlying mechanism that involves lysosomal Ca2+ release

Oh,

Park,

Sonn

et al. 2023

Exp Mol Med

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“…To avoid potential oxygen limitation, all experiments were carried out under hyperoxygenated conditions and followed a previously described protocols ( Rocha et al, 2018 ; Kuznetsov et al, 2008 ; Sahl et al, 2021 ). Twenty minutes prior to the addition of substrates, CL was provided to the 2 mL oxygraph chambers for a final concentration of 1 and 10 μM, respectively.…”

Section: Methodsmentioning

confidence: 99%

Physiological levels of cardiolipin acutely affect mitochondrial respiration in vascular smooth muscle cells

Galambo¹,

Bergdahl²

2023

Current Research in Physiology

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Lysosomal Ca2+-mediated TFEB activation modulates mitophagy and functional adaptation of pancreatic β-cells to metabolic stress

Park¹,

Lim²,

Kim³

et al. 2022

Nat Commun

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Although autophagy is critical for pancreatic β-cell function, the role and mechanism of mitophagy in β-cells are unclear. We studied the role of lysosomal Ca2+ in TFEB activation by mitochondrial or metabolic stress and that of TFEB-mediated mitophagy in β-cell function. Mitochondrial or metabolic stress induced mitophagy through lysosomal Ca2+ release, increased cytosolic Ca2+ and TFEB activation. Lysosomal Ca2+ replenishment by ER- > lysosome Ca2+ refilling was essential for mitophagy. β-cell-specific Tfeb knockout (TfebΔβ-cell) abrogated high-fat diet (HFD)-induced mitophagy, accompanied by increased ROS and reduced mitochondrial cytochrome c oxidase activity or O2 consumption. TfebΔβ-cell mice showed aggravation of HFD-induced glucose intolerance and impaired insulin release. Metabolic or mitochondrial stress induced TFEB-dependent expression of mitophagy receptors including Ndp52 and Optn, contributing to the increased mitophagy. These results suggest crucial roles of lysosomal Ca2+ release coupled with ER- > lysosome Ca2+ refilling and TFEB activation in mitophagy and maintenance of pancreatic β-cell function during metabolic stress.

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Cardiac mitochondrial respiration following a low-carbohydrate, high-fat diet in apolipoprotein E-deficient mice

Cited by 4 publications

References 34 publications

Pancreatic β-cell mitophagy as an adaptive response to metabolic stress and the underlying mechanism that involves lysosomal Ca2+ release

Pancreatic β-cell mitophagy as an adaptive response to metabolic stress and the underlying mechanism that involves lysosomal Ca2+ release

Physiological levels of cardiolipin acutely affect mitochondrial respiration in vascular smooth muscle cells

Lysosomal Ca2+-mediated TFEB activation modulates mitophagy and functional adaptation of pancreatic β-cells to metabolic stress

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