Fuel selection by the kidney: adaptation to starvation

Baverel, Gabriel; Ferrier, Bernard; Martin, Marielle

doi:10.1079/pns19950049

Cited by 12 publications

(7 citation statements)

References 102 publications

(156 reference statements)

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“…Among these, fatty acid transport protein is expressed in the rat kidney cortex, and we recently showed that fatty acid transport protein gene expression is upregulated by high-fat feeding or by administration of clofibrate (20). Whatever mechanism is involved, it is known that renal uptake of fatty acids can vary according to changes in the plasma level of these substrates (2). Our data therefore suggest that such changes in cellular fatty acid flux, even when relatively modest, could have direct short-term effects on fatty acid ␤-oxidation enzyme gene expression.…”

Section: Discussionmentioning

confidence: 99%

Effects of fatty acids on mitochondrial β-oxidation enzyme gene expression in renal cell lines

Ouali

Djouadi

Bastin

2002

American Journal of Physiology-Renal Physiology

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Regulatory effects of fatty acids on gene expression of medium-chain acyl-CoA dehydrogenase (MCAD), a mitochondrial β-oxidation enzyme, were investigated in rabbit kidney cell lines derived from proximal tubule (RC.SV1), thick ascending limb of Henle's loop (RC.SV2), or collecting duct (RC.SV3). Exposure to long-chain fatty acids led to significant increases (2-fold) in MCAD mRNA abundance in RC.SV1 and RC.SV2 cells; kinetics and dose-response studies established that maximal MCAD gene stimulation was reached 4 h after addition of 50 μM oleate (C18:1) in the culture medium. These effects of fatty acids were totally abolished in the presence of 1 μg/ml actinomycin D, a transcription inhibitor. Staining of cellular lipids revealed that fatty acid-induced gene stimulation could occur in the absence of cellular fatty acid accumulation. Altogether, these data indicate that small changes in cellular fatty acid flux can have direct short-term effects on fatty acid oxidation enzyme gene expression in renal cells, and this might take part in the regulation of cellular fatty acid homeostasis in response to changes in tubular fluid composition.

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Section: Discussionmentioning

confidence: 99%

Effects of fatty acids on mitochondrial β-oxidation enzyme gene expression in renal cell lines

Ouali

Djouadi

Bastin

2002

American Journal of Physiology-Renal Physiology

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“…The kidney has long been the subject of metabolic studies (52)(53)(54)(55)(56). It has the capacity to metabolize a large variety of substrates (e.g.…”

Section: Discussionmentioning

confidence: 99%

Reduction of Proteinuria through Podocyte Alkalinization

Altintas

Moriwaki

Wei

et al. 2014

Journal of Biological Chemistry

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Background: Podocyte injury can be caused by cytosolic cathepsin L activity, leading to foot process effacement and proteinuria. Results: Glutamine blunts the damaging activity of induced cytosolic cathepsin L in podocytes by modulating intracellular pH. Conclusion: Podocyte pH modulation is a novel way to tackle proteinuric kidney disease. Significance: The optimization of amino acid metabolism fluxes and associated pH i of podocytes may form a basis for novel therapeutic approaches.

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“…At rest, the healthy heart and kidney cortex rely mainly on fatty acid oxidation ( Figure 1 ). ( Baverel et al, 1995 ; Lopaschuk et al, 2020 ; Dong et al, 2021 ; Wen et al, 2021 ) Macrophage metabolic reprogramming involves distinct changes in the mitochondrial TCA cycle, which is influenced by glucose and fatty acid oxidation ( Zhang et al, 2019b ; Viola et al, 2019 ). In inflammatory macrophages, the TCA cycle is truncated at key points to allow accumulation of key metabolites, in particular succinate and itaconate ( Viola et al, 2019 ).…”

Section: Roles Of Conventional Fuels During Cardiorenal Injurymentioning

confidence: 99%

“…Given the rise in popularity of low-carbohydrate/ketogenic diets, many recent studies have focused on the roles and potential therapeutic effects of the major ketone bodies, including beta-hydroxybutyrate (BHB) and acetoacetate (AA) ( Abbasi, 2018 ). Both the heart and kidneys are capable of metabolizing ketones during starvation or consumption of ketogenic diets, and consume exogenously infused ketones in humans ( Baverel et al, 1995 ; Mizuno et al, 2017 ; Puchalska and Crawford, 2017 ; Cuenoud et al, 2020 ; Lopaschuk et al, 2020 ). During injury, the heart and kidneys can increase ketone oxidation as an adaptation to chronic pathological stress ( Figure 1 ).…”

Section: Potential Roles Of Alternative Fuels During Cardiorenal Injurymentioning

confidence: 99%

Targeting immunometabolism during cardiorenal injury: roles of conventional and alternative macrophage metabolic fuels

et al. 2023

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Macrophages play critical roles in mediating and resolving tissue injury as well as tissue remodeling during cardiorenal disease. Altered immunometabolism, particularly macrophage metabolism, is a critical underlying mechanism of immune dysfunction and inflammation, particularly in individuals with underlying metabolic abnormalities. In this review, we discuss the critical roles of macrophages in cardiac and renal injury and disease. We also highlight the roles of macrophage metabolism and discuss metabolic abnormalities, such as obesity and diabetes, which may impair normal macrophage metabolism and thus predispose individuals to cardiorenal inflammation and injury. As the roles of macrophage glucose and fatty acid metabolism have been extensively discussed elsewhere, we focus on the roles of alternative fuels, such as lactate and ketones, which play underappreciated roles during cardiac and renal injury and heavily influence macrophage phenotypes.

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Fuel selection by the kidney: adaptation to starvation

Cited by 12 publications

References 102 publications

Effects of fatty acids on mitochondrial β-oxidation enzyme gene expression in renal cell lines

Effects of fatty acids on mitochondrial β-oxidation enzyme gene expression in renal cell lines

Reduction of Proteinuria through Podocyte Alkalinization

Targeting immunometabolism during cardiorenal injury: roles of conventional and alternative macrophage metabolic fuels

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