Effects of oral butyrate supplementation on inflammatory potential of circulating peripheral blood mononuclear cells in healthy and obese males

Cleophas, Maartje C. P.; Ratter, Jacqueline M.; Bekkering, Siroon; Quintin, Jessica; Schraa, Kiki; Stroes, Erik S.G.; Netea, Mihai G.; Joosten, Leo A. B.

doi:10.1038/s41598-018-37246-7

Cited by 89 publications

(71 citation statements)

References 38 publications

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“…Since then, U.S. dietary guidelines have remained steadfast in their recommendation to substitute fat-free or low-fat dairy for higher-fat dairy products [6]. Mounting evidence, however, supports that the “diet-heart hypothesis” is an oversimplification of dietary saturated fat and that health effects of saturated fat are considerably dependent upon other important factors, such as food source and matrix [33], the overall dietary pattern of an individual, and the health status of the individual [34,35]. Paradoxically, despite a more thorough understanding of the heterogenous health effects of dietary SFA, dietary guidelines outside of the U.S. also continue to discourage full-fat dairy products (Figure 1).…”

Section: Dairy-derived Sfa Intake Recommendations In Dietary Guidementioning

confidence: 99%

“…Moreover, studies have shown that differences in food matrix, even within types of dairy products, can modify cardiometabolic risk [128]. Another important consideration is that studies focused on the effects of the consumption of single nutrients often evaluate a very high amount of the nutrient of interest (e.g., 4 g/d butyrate [34,35]). Future research should carefully consider the concentration of a single nutrient that may be attained in an average, balanced diet to enhance the study design’s applicability.…”

Section: Potential Mechanisms Driving Differential Effects Of Sfa mentioning

confidence: 99%

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Dairy Fat Consumption and the Risk of Metabolic Syndrome: An Examination of the Saturated Fatty Acids in Dairy

2019

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Lifestyle is a key modifiable risk factor involved in the manifestation of metabolic syndrome and, in particular, diet plays a pivotal role in its prevention and development. Current dietary guidelines discourage the consumption of saturated fat and dietary sources rich in saturated fat, such as dairy products, despite data suggesting that full-fat dairy consumption is protective against metabolic syndrome. This narrative review assessed the recent epidemiological and clinical research that examined the consumption of dairy-derived saturated fatty acids (SFA) on metabolic syndrome risk. In addition, this review evaluated studies of individual SFA to gain insight into the potential mechanisms at play with intake of a diet enriched with these dairy-derived fatty acids. This work underscores that SFA are a heterogenous class of fatty acids that can differ considerably in their biological activity within the body depending on their length and specific chemical structure. In summary, previous work on the impact of dairy-derived SFA consumption on disease risk suggests that there is currently insufficient evidence to support current dietary guidelines which consolidate all dietary SFA into a single group of nutrients whose consumption should be reduced, regardless of dietary source, food matrix, and composition.

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Section: Dairy-derived Sfa Intake Recommendations In Dietary Guidementioning

confidence: 99%

Section: Potential Mechanisms Driving Differential Effects Of Sfa mentioning

confidence: 99%

Dairy Fat Consumption and the Risk of Metabolic Syndrome: An Examination of the Saturated Fatty Acids in Dairy

2019

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“…In the early 1980s, it was reported that short-chain fatty acids possess therapeutic potential in some forms of colitis [12], which has since been in part confirmed in animal and human studies for Crohn's disease. Recently, oral butyrate supplementation was reported to decrease cytokine release in patients with metabolic syndrome [13]. In addition, studies also suggest that an oral supplementation of therapeutic doses of sodium butyrate (SoB) (0.2-0.6 g/kg bw/d) may attenuate insulin resistance and the development of NAFLD, e.g., steatosis, inflammation and even early signs of fibrosis in rodents [6,[14][15][16].…”

Section: Introductionmentioning

confidence: 99%

Oral Supplementation of Sodium Butyrate Attenuates the Progression of Non-Alcoholic Steatohepatitis

et al. 2020

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Sodium butyrate (SoB) supplementation has been suggested to attenuate the development of non-alcoholic fatty liver disease (NAFLD). Here, we determined the therapeutic potential of SoB on NAFLD progression and molecular mechanism involved. Eight-week old C57BL/6J mice were pair-fed a fat-, fructose- and cholesterol-rich diet (FFC) or control diet (C). After 8 weeks, some mice received 0.6g SoB/kg bw in their respective diets (C+SoB; FFC+SoB) or were maintained on C or FFC for the next 5 weeks of feeding. Liver damage, markers of glucose metabolism, inflammation, intestinal barrier function and melatonin metabolism were determined. FFC-fed mice progressed from simple steatosis to early non-alcoholic steatohepatitis, along with significantly higher TNFα and IL-6 protein levels in the liver and impaired glucose tolerance. In FFC+SoB-fed mice, disease was limited to steatosis associated with protection against the induction of Tlr4 mRNA and iNOS protein levels in livers. SoB supplementation had no effect on FFC-induced loss of tight junction proteins in the small intestine but was associated with protection against alterations in melatonin synthesis and receptor expression in the small intestine and livers of FFC-fed animals. Our results suggest that the oral supplementation of SoB may attenuate the progression of simple steatosis to steatohepatitis.

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“…For example, monocytes derived from humans with high levels of Lipoprotein A(Lpa), a cardiovascular risk factor that carries oxidized phospholipids, have increased capacity of producing pro-inflammatory cytokines upon stimulation and this is phenotype is also observed in macrophages from healthy individuals treated with oxidized LDL (68, 81, 82). Oral supplementation with the metabolic byproduct butyrate, also decreases training of peripheral mononuclear macrophages by oxidized LDL in obese humans with metabolic syndrome (83).…”

Section: Introductionmentioning

confidence: 99%

Insulin Signaling and Insulin Resistance Facilitate Trained Immunity in Macrophages Through Metabolic and Epigenetic Changes

et al. 2019

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Adaptation of the innate immune system has been recently acknowledged, explaining sustained changes of innate immune responses. Such adaptation is termed trained immunity. Trained immunity is initiated by extracellular signals that trigger a cascade of events affecting cell metabolism and mediating chromatin changes on genes that control innate immune responses. Factors demonstrated to facilitate trained immunity are pathogenic signals (fungi, bacteria, viruses) as well non-pathogenic signals such as insulin, cytokines, adipokines or hormones. These signals initiate intracellular signaling cascades that include AKT kinases and mTOR as well as histone methylases and demethylases, resulting in metabolic changes and histone modifications. In the context of insulin resistance, AKT signaling is affected resulting in sustained activation of mTORC1 and enhanced glycolysis. In macrophages elevated glycolysis readily impacts responses to pathogens (bacteria, fungi) or danger signals (TLR-driven signals of tissue damage), partly explaining insulin resistance-related pathologies. Thus, macrophages lacking insulin signaling exhibit reduced responses to pathogens and altered metabolism, suggesting that insulin resistance is a state of trained immunity. Evidence from Insulin Receptor as well as IGF1Receptor deficient macrophages support the contribution of insulin signaling in macrophage responses. In addition, clinical evidence highlights altered macrophage responses to pathogens or metabolic products in patients with systemic insulin resistance, being in concert with cell culture and animal model studies. Herein, we review the current knowledge that supports the impact of insulin signaling and other insulin resistance related signals as modulators of trained immunity.

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Effects of oral butyrate supplementation on inflammatory potential of circulating peripheral blood mononuclear cells in healthy and obese males

Cited by 89 publications

References 38 publications

Dairy Fat Consumption and the Risk of Metabolic Syndrome: An Examination of the Saturated Fatty Acids in Dairy

Dairy Fat Consumption and the Risk of Metabolic Syndrome: An Examination of the Saturated Fatty Acids in Dairy

Oral Supplementation of Sodium Butyrate Attenuates the Progression of Non-Alcoholic Steatohepatitis

Insulin Signaling and Insulin Resistance Facilitate Trained Immunity in Macrophages Through Metabolic and Epigenetic Changes

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