Intermittent Fasting as Possible Treatment for Heart Failure

Garza-González, Salvador; Nieblas, Bianca; Solbes-Gochicoa, María M.; Altamirano, Julio; Garcı́a, Noemı́

doi:10.2174/1570161120666220610151915

Cited by 8 publications

(4 citation statements)

References 104 publications

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“…Fasting (including intermittent fasting and time-restricted feeding), is an established trigger of ketosis, which increases the preference for KBs as energy substrates in human tissues 19,32 . Beneficial effects of fasting in various pathological conditions have been at least partially attributed to increased ketonemia 33 . As a proof of concept, we compared HBA-driven respiration in mice fasted for 16 h with mice with continuous access to normal chow and found a greater JO 2 in livers of fasted mice (Figure 3D).…”

Section: Resultsmentioning

confidence: 99%

High-resolution respirometry reveals altered mammalian tissue ketone body oxidation in different cardiometabolic diseases

Zweck,

Piel,

Schmidt

et al. 2024

Preprint

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SummaryAbnormal mitochondrial oxidative phosphorylation (OXPHOS) is key to the pathogenesis of several cardiometabolic diseases. The ketone bodies (KBs), β-hydroxybutyrate (HBA) and acetoacetate (ACA), are critical for tissue-specific energy metabolism under various pathophysiological conditions. However, robust methods quantifying their contribution as substrates for OXPHOS are lacking. Here, we first established comprehensive high-resolution respirometry protocols for assessing the differential contributions of HBA, ACA, and related ketolytic enzymes to OXPHOS in translational studies in mice and humans. We then utilized these protocols to demonstrate (i) organ-specific differences in KB-driven mitochondrial respiration in mice, (ii) lower KB-driven mitochondrial respiration in liver of humans with steatosis, skeletal muscle of humans with diabetes and in kidney of diet-induced obese mice, as well as (iii) higher mitochondrial KB utilization capacity in mouse and human failing heart. These results highlight organ-specific roles of KB metabolism in cardiometabolic diseases and shall help to identify novel targets in these pathways.

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Section: Resultsmentioning

confidence: 99%

High-resolution respirometry reveals altered mammalian tissue ketone body oxidation in different cardiometabolic diseases

Zweck,

Piel,

Schmidt

et al. 2024

Preprint

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“…In addition, IF is believed to have great potential in improving long-term health. Studies have shown that IF can reduce weight and have an effect on heart protection (33,34) . This protective effect may be related to decreased lipid deposition, increased adiponectin concentration and decreased leptin and LDL concentrations (35) .…”

Section: Discussionmentioning

confidence: 99%

Intermittent fasting promotes adipocyte mitochondrial fusion through Sirt3-mediated deacetylation of Mdh2

Liang

Tian

et al. 2023

Br J Nutr

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Fat deposition and lipid metabolism are closely related to the morphology, structure and function of mitochondria. The morphology of mitochondria between fusion and fission processes is mainly regulated by protein posttranslational modification (PTM). Intermittent fasting (IF) promotes high expression of Sirtuin 3 (Sirt3) and induces mitochondrial fusion in high-fat diet (HFD)-fed mice. However, the mechanism by which Sirt3 participates in mitochondrial protein acetylation during IF to regulate mitochondrial fusion and fission dynamics remains unclear. This article demonstrates that IF promotes mitochondrial fusion and improves mitochondrial function in HFD mouse inguinal white adipose tissue (iWAT). Proteomic sequencing revealed that IF increased protein deacetylation levels in HFD mice and significantly increased Sirt3 mRNA and protein expression. After transfecting with Sirt3 overexpression or interference vectors into adipocytes, we found that Sirt3 promoted adipocyte mitochondrial fusion and improved mitochondrial function. Furthermore, Sirt3 regulates the JNK-FIS1 pathway by deacetylating malate dehydrogenase 2 (MDH2) to promote mitochondrial fusion. In summary, our study indicates that IF promotes mitochondrial fusion and improves mitochondrial function by upregulating the high expression of Sirt3 in HFD mice, promoting deacetylation of MDH2, and inhibiting the JNK-FIS1 pathway. This research provides theoretical support for studies related to energy limitation and animal lipid metabolism.

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“…A western-style diet often leads to food overconsumption, which triggers the development of comorbidities such as obesity, hypercholesterolemia, cardiovascular disease, and chronic heart failure. Several studies suggest that intermittent fasting may also protect against the development of those morbidities [16]. Interestingly, it has been shown that fasting may be related to the modulation of autophagy and/or mitophagy [17].…”

Section: Introductionmentioning

confidence: 99%

Exogenous and Endogenous Molecules Potentially Proficient to Modulate Mitophagy in Cardiac Disorders

Nakashima,

Suga,

Matsuda

2024

Kinases and Phosphatases

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It has been proposed that procedures which upregulate mitochondrial biogenesis and autophagy by replacing damaged mitochondria with healthy ones may prevent the development of several heart diseases. A member of serine and threonine kinases, adenosine monophosphate-activated protein kinase (AMPK), could play essential roles in the autophagy and/or mitophagy. AMPK is widely distributed in various cells, which might play diverse regulatory roles in different tissues and/or organs. In fact, changes in the kinase function of AMPK due to alteration of activity have been linked with diverse pathologies including cardiac disorders. AMPK can regulate mitochondrial biogenesis via peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) signaling and also improve oxidative mitochondrial metabolism through inhibition of mechanistic/mammalian target of rapamycin (mTOR) pathway, which may also modulate the autophagy/mitophagy through autophagy activating kinase 1 (ULK1) and/or transforming growth factor beta (TGF-β) signaling. Therefore, the modulation of AMPK in autophagy/mitophagy pathway might probably be thought as a therapeutic tactic for several cardiac disorders. As kinases are amongst the most controllable proteins, in general, the design of small molecules targeting kinases might be an eye-catching avenue to modulate cardiac function. Some analyses of the molecular biology underlying mitophagy suggest that nutraceuticals and/or drugs including specific AMPK modulator as well as physical exercise and/or dietary restriction that could modulate AMPK may be useful against several heart diseases. These observations may virtually be limited to preclinical studies. Come to think of these, however, it is speculated that some nutraceutical regimens might have positive potential for managing some of cardiac disorders.

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Intermittent Fasting as Possible Treatment for Heart Failure

Cited by 8 publications

References 104 publications

High-resolution respirometry reveals altered mammalian tissue ketone body oxidation in different cardiometabolic diseases

High-resolution respirometry reveals altered mammalian tissue ketone body oxidation in different cardiometabolic diseases

Intermittent fasting promotes adipocyte mitochondrial fusion through Sirt3-mediated deacetylation of Mdh2

Exogenous and Endogenous Molecules Potentially Proficient to Modulate Mitophagy in Cardiac Disorders

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