Sodium butyrate recovers high-fat diet-fed female Wistar rats from glucose dysmetabolism and uric acid-associated cardiac tissue damage

Badejogbin, Caroline; Areola, D.E; Olaniyi, Kehinde S.; Adeyanju, O.; Adeosun, Isaac O

doi:10.1007/s00210-019-01679-2

Cited by 29 publications

(15 citation statements)

References 28 publications

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“…The findings of both in vivo and in vitro experiments show that butyrate exerts histological cardio-protective effects. Badejogbin et al examined the impact of SB (200 mg/kg) on heart tissue damage in rats fed either chow or high fat diet (HFD) ( Badejogbin et al, 2019 ). In that research, butyrate significantly ameliorated HFD induced cardio-metabolic abnormalities including hyperlipidemia and glucose dysmetabolism as well as elevated plasma malondialdehyde, corticosterone, and lactate dehydrogenase ( Badejogbin et al, 2019 ).…”

Section: The Effects Of Butyrate On Cvdmentioning

confidence: 99%

“…Badejogbin et al examined the impact of SB (200 mg/kg) on heart tissue damage in rats fed either chow or high fat diet (HFD) ( Badejogbin et al, 2019 ). In that research, butyrate significantly ameliorated HFD induced cardio-metabolic abnormalities including hyperlipidemia and glucose dysmetabolism as well as elevated plasma malondialdehyde, corticosterone, and lactate dehydrogenase ( Badejogbin et al, 2019 ). Furthermore, the histological study revealed that butyrate improved cardiac tissue infarction, infiltration, and fibrosis.…”

Section: The Effects Of Butyrate On Cvdmentioning

confidence: 99%

“…Furthermore, the histological study revealed that butyrate improved cardiac tissue infarction, infiltration, and fibrosis. Butyrate has been shown to protect cardiac tissue architecture and integrity by lowering uric acid (plasma and cardiac tissue) and increasing glutathione antioxidant defenses ( Badejogbin et al, 2019 ).…”

Section: The Effects Of Butyrate On Cvdmentioning

confidence: 99%

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Role of Butyrate, a Gut Microbiota Derived Metabolite, in Cardiovascular Diseases: A comprehensive narrative review

et al. 2022

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Cardiovascular diseases (CVD) are major causes of death worldwide. Recently, new roles for intestinal microbiota in pathology and treatment of CVD have been proposed. Butyrate, a bacterial metabolite, is synthesized in the gut and performs most of its functions in there. However, researchers have discovered that butyrate could enter to portal vein and interact with various organs. Butyrate exhibits a broad range of pharmacological activities, including microbiome modulator, anti-inflammatory, anti-obesity, metabolic pathways regulator, anti-angiogenesis, and antioxidant. In this article we review evidence supporting a potentially therapeutic role for butyrate in CVD and the mechanisms and pathways involved in the cardio-protective effects of butyrate from the gut and circulation to the nervous system. In summary, although butyrate exhibits a wide variety of biological activities in different pathways including energy homeostasis, glucose and lipid metabolism, inflammation, oxidative stress, neural signaling, and epigenetic modulation in experimental settings, it remains unclear whether these findings are clinically relevant and whether the molecular pathways are activated by butyrate in humans.

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Section: The Effects Of Butyrate On Cvdmentioning

confidence: 99%

Section: The Effects Of Butyrate On Cvdmentioning

confidence: 99%

Section: The Effects Of Butyrate On Cvdmentioning

confidence: 99%

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Role of Butyrate, a Gut Microbiota Derived Metabolite, in Cardiovascular Diseases: A comprehensive narrative review

et al. 2022

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“…In terms of the role of butyrate in heart, butyrate improves cardiac function and suppresses myocardial remodeling in the diabetic heart via inhibiting HDAC activity and enhancing the expression of superoxide dismutase (SOD1) [117]. Meanwhile, butyrate can protect against high-fat diet (HFD)-induced cardiac dysfunction and uric acid-associated cardiac tissue damage through repression of uric acid (UA) and augmentation of glutathione antioxidant defenses [118]. Treatment with butyrate attenuates fractional abdominal aorta ligation-stimulated myocardial hypertrophy, as confirmed by reduced collagen content and preservation of left ventricle systolic and diastolic dysfunction through reducing oxidative stress and increasing mitochondrial DNA concentration [119].…”

Section: Butyrate and Butyrylationmentioning

confidence: 99%

Short-chain fatty acid, acylation and cardiovascular diseases

2020

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Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide. Metabolic dysfunction is a fundamental core mechanism underlying CVDs. Previous studies generally focused on the roles of long-chain fatty acids (LCFAs) in CVDs. However, a growing body of study has implied that short-chain fatty acids (SCFAs: namely propionate, malonate, butyrate, 2-hydroxyisobutyrate (2-HIBA), β-hydroxybutyrate, crotonate, succinate, and glutarate) and their cognate acylations (propionylation, malonylation, butyrylation, 2-hydroxyisobutyrylation, β-hydroxybutyrylation, crotonylation, succinylation, and glutarylation) participate in CVDs. Here, we attempt to provide an overview landscape of the metabolic pattern of SCFAs in CVDs. Especially, we would focus on the SCFAs and newly identified acylations and their roles in CVDs, including atherosclerosis, hypertension, and heart failure. Clinical Science (2020) 134 657-676 https://doi.org/10.1042/CS20200128 cofactors in certain protein acylations, such as propionylation [14], malonylation [15], butyrylation [14], 2-hydroxyisobutyrylation [16], β-hydroxybutyrylation [17], crotonylation [18], succinylation [19], and glutarylation [20]. These discoveries give us a deeper understanding of PTM. Among PTMs, protein acetylation is the earliest discovered and most studied. Similar to protein acetylation, various studies have shown that these newly discovered PTMs are also involved in physiological and pathophysiological processes, including cardiovascular homeostasis.Here in this review, we will summarize SCFAs, protein acylations, and their emerging roles in CVDs, including atherosclerosis, hypertension, and heart failure. The metabolic pattern and FAs in CVDsThe heart is an 'omnivore' , using FAs, glucose, lactate, ketone bodies, and amino acids as metabolic substrates [5,6]. The substrates utilized by the embryonic heart are significantly different from those used by the adult heart. The embryonic heart depends primarily on glycolysis as well as lactate oxidation to produce energy [21]. The newborn and adult heart shift toward the remarkable utilization of FAs to meet cardiac energy demand [5,9]. In failing hearts, a decrease in FA oxidation and an increase in glycolysis are critically involved in cardiac dysfunction [22]. As thus, the metabolic pattern is essential for maintaining cardiac and vascular functions.Diabetes, hypertension, and obesity contribute to heart failure syndrome. Accumulating evidence suggests that hypertension, ischemic hearts, and heart failure induce a shift in substrate toward the remarkable utilization of glucose to generate energy. Despite this shift, the FA oxidation remains to make much energy for the diseased heart [23]. Since FAs are the predominant substrates for cardiomyocytes, alterations in FA metabolism have been implicated as causal in cardiac diseases. FAs within cells and in the circulation are critically involved in cardiometabolic diseases. CVDs are closely associated with lifestyle and metabolic status, which affect circul...

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“…Rats provided with butyrate in the diet exhibited significantly improved energy metabolism of the heart, reduced myocardial infarction, decreased fat infiltration and reduced fibrosis caused by the high‐fat diet, and an increased plasma content of reduced glutathione (Badejogbin et al . 2019). After intra‐abdominal injection of butyrate in rats with myocardial infarction, the area of infarction was diminished.…”

Section: Effects Of Butyrate On Asmentioning

confidence: 99%

Role and mechanism of action of butyrate in atherosclerotic diseases: a review

Yang

Guo

et al. 2021

J Appl Microbiol

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Butyrate is a bioactive molecule produced by the intestinal flora and plays a major role in a variety of inflammatory diseases. Increasing evidence indicates that butyrate can regulate the occurrence and development of atherosclerosis. Coincidentally, it reduces hyperlipidemia and hyperglycemia, which are major risk factors of atherosclerosis. However, the mechanism by which butyrate regulates the development of atherosclerosis remains unclear. In this article, we review the effect of butyrate treatment on atherosclerosis with a focus on the mechanisms of butyrate-mediated modulation of several atherosclerotic processes. These include the improvement of monocyte-endothelial interactions, macrophage lipid accumulation, smooth muscle cell proliferation and migration, and lymphocyte differentiation and function. The existing research indicates that butyrate treatment may be a potentially effective strategy for the prevention of atherosclerosis. Identity and underlying mechanisms of the molecular pathways of these interactions should be explored in the future to counter atherosclerosis effectively.

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Sodium butyrate recovers high-fat diet-fed female Wistar rats from glucose dysmetabolism and uric acid-associated cardiac tissue damage

Cited by 29 publications

References 28 publications

Role of Butyrate, a Gut Microbiota Derived Metabolite, in Cardiovascular Diseases: A comprehensive narrative review

Role of Butyrate, a Gut Microbiota Derived Metabolite, in Cardiovascular Diseases: A comprehensive narrative review

Short-chain fatty acid, acylation and cardiovascular diseases

Role and mechanism of action of butyrate in atherosclerotic diseases: a review

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