Propionic acid and butyric acid inhibit lipolysis and de novo lipogenesis and increase insulin-stimulated glucose uptake in primary rat adipocytes

Heimann, Emilia; Nyman, Margareta; Degerman, Eva

doi:10.4161/21623945.2014.960694

Cited by 94 publications

(66 citation statements)

References 54 publications

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“…The finding that isobutyric acid significantly increased both basal and insulin-stimulated glucose uptake is in agreement with recently obtained results for propionic acid and to some extent also for butyric acid in rodent primary and differentiated adipocytes 33 . Phosphorylation of PKB is one key event in insulin-induced glucose uptake, 41 however, phosphorylation of PKB was shown to be downregulated by both branched and non-branched SCFAs.…”

Section: Discussionsupporting

confidence: 92%

“…The finding that BSCFAs decrease the rate of de novo lipogenesis, 54 measured as the incorporation of [ 3 H]-labeled glucose into cellular lipids, is in agreement with previous results with non-branched SCFAs 33 . Altogether, these findings indicate that BSCFAs and SCFAs facilitate storage of diet-derived lipids in adipocytes rather than performing de novo synthesis, which at least under conditions of fat over-consumption appears metabolically beneficial.…”

Section: Discussionsupporting

confidence: 91%

“…The finding that isobutyric and isovaleric acid inhibited isoproterenol-mediated lipolysis and decreased isoproterenol-induced phosphorylation of HSL, indicate a role for BSCFAs in the regulation of energy homeostasis by protecting against lipotoxicity, as has previously been reported for SCFAs 33-35 . Importantly, the mechanism behind the anti-lipolytic effect of BSCFAs and SCFAs appears not to involve components utilized by insulin to mediate inhibition of lipolysis.…”

Section: Discussionsupporting

confidence: 57%

“…Also, the effect to diminish de novo lipogenesis might lead to an increased β-oxidation due to reduced level of malonyl CoA, a metabolite known to inhibit the transport of fatty acids into the mitochondria 55 . The inhibitory effect on PKB phosphorylation observed in response to the branched and non-branched SCFAs and the phosphorylation and inactivation of ACC 33 might be molecular mechanisms for diminished de novo lipogenesis. Isovaleric acid-containing porpoise oil, given in the diet, has ameliorating effects on fatty liver in OLETF (Otsuka Long- Evans Tokushima Fatty) rat, a model for type 2 diabetes, by increasing serum levels of adiponectin and enhancing lipoprotein synthesis and secretion 56 .…”

Section: Discussionmentioning

confidence: 99%

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Branched short-chain fatty acids modulate glucose and lipid metabolism in primary adipocytes

et al. 2016

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Short-chain fatty acids (SCFAs), e.g. acetic acid, propionic acid and butyric acid, generated through colonic fermentation of dietary fibers, have been shown to reach the systemic circulation at micromolar concentrations. Moreover, SCFAs have been conferred anti-obesity properties in both animal models and human subjects. Branched SCFAs (BSCFAs), e.g., isobutyric and isovaleric acid, are generated by fermentation of branched amino acids, generated from undigested protein reaching colon. However, BSCFAs have been sparsely investigated when referring to effects on energy metabolism. Here we primarily investigate the effects of isobutyric acid and isovaleric acid on glucose and lipid metabolism in primary rat and human adipocytes. BSCFAs inhibited both cAMP-mediated lipolysis and insulin-stimulated de novo lipogenesis at 10 mM, whereas isobutyric acid potentiated insulin-stimulated glucose uptake by all concentrations (1, 3 and 10 mM) in rat adipocytes. For human adipocytes, only SCFAs inhibited lipolysis at 10 mM. In both in vitro models, BSCFAs and SCFAs reduced phosphorylation of hormone sensitive lipase, a rate limiting enzyme in lipolysis. In addition, BSCFAs and SCFAs, in contrast to insulin, inhibited lipolysis in the presence of wortmannin, a phosphatidylinositide 3-kinase inhibitor and OPC3911, a phosphodiesterase 3 inhibitor in rat adipocytes. Furthermore, BSCFAs and SCFAs reduced insulin-mediated phosphorylation of protein kinase B. To conclude, BSCFAs have effects on adipocyte lipid and glucose metabolism that can contribute to improved insulin sensitivity in individuals with disturbed metabolism.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

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Branched short-chain fatty acids modulate glucose and lipid metabolism in primary adipocytes

et al. 2016

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“…Previous studies suggested that in addition to effects on skeletal muscle and liver metabolism, microbial products might affect lipid storage [6,7] and lipolysis [8,9] in the adipose tissue. External alterations of the gut microbiota composition (i.e.…”

Section: Introductionmentioning

confidence: 99%

Effects of gut microbiota manipulation onex vivolipolysis in human abdominal subcutaneous adipocytes

Jocken¹,

Reijnders

Canfora³

et al. 2018

Adipocyte

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The intestinal microbiota may contribute to the development of obesity by affecting host lipid metabolism and insulin sensitivity. To investigate the effects of microbiota manipulation on ex vivo basal and β-adrenergically-stimulated lipolysis in human adipocytes, 36 obese men were randomized to amoxicillin (broad-spectrum antibiotic), vancomycin (narrow-spectrum antibiotic) or placebo treatment (7 d, 1500 mg/d). Before and after treatment, ex vivo adipose tissue lipolysis was assessed under basal conditions and during stimulation with the non-selective β-agonist isoprenaline using freshly isolated mature adipocytes. Gene (targeted microarray) and protein expression were analyzed to investigate underlying pathways.Antibiotics treatment did not significantly affect basal and maximal isoprenaline-mediated glycerol release from adipocytes. Adipose tissue β-adrenoceptor expression or post-receptor signalling was also not different between groups. In conclusion, 7 d oral antibiotics treatment has no effect on ex vivo lipolysis in mature adipocytes derived from adipose tissue of obese insulin resistant men.

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Arctigenin improves lipid metabolism by regulating AMP‐activated protein kinase and downstream signaling pathways

Yuzhou

Liu

et al. 2019

J of Cellular Biochemistry

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Although it has been reported that arctigenin (ARG) can reduce the body weight and inhibit adipogenic differentiation by activating AMP-activated protein kinase (AMPK), the exact signals responsible for the ARG-mediated antiobesity mechanism through AMPK are not well understood. In this study, we investigated the potential improvement of AGR on lipid metabolism using a high-fat diet (HFD)-induced hyperlipidemia rats and 3T3-L1 mature adipocytes.The levels of AMPK and its downstream factors were examined by Western blot analysis and real-time fluorescent quantitative polymerase chain reaction. We observed that ARG lowered the HFD-induced body weight and the levels of serum lipid. Moreover, ARG clearly alleviated fat deposition in the liver and reduced epididymal fat accumulation. ARG also suppressed lipogenesis and lipolysis but promoted fatty acid β-oxidation in adipocytes. Most importantly, ARG increased the phosphorylation of AMPK and acetyl-CoA carboxylase (ACC) and upregulated the messenger RNA levels of downstream genes related to fatty acid β-oxidation, such as carnitine palmitoyltransferase 1 and acyl-CoA oxidase 1 but downregulated the expression of peroxisome proliferator-activated receptor γ (PPARγ), sterol regulatory element-binding transcription factor 1 (SREBP1c) and their targets, including lipogenesis-related genes such as CCAAT/enhancer-binding protein α, lipoprotein lipase, adipocyte protein 2, and fatty acid synthase (FAS), as well as lipolysis-related genes such as adipose triglyceride lipase and hormone-sensitive lipase. The activity of FAS was also decreased by ARG. We conclude that AMPK activation is important for the pharmacological effects of ARG. ARG may improve lipid metabolism by regulating the AMPK-ACC and AMPK-PPARγ/SREBP1c signaling pathways. K E Y W O R D S3T3-L1 adipocyte, AMP-activated protein kinase, arctigenin, fatty acid β-oxidation, HFD-induced hyperlipidemia SD rats, lipogenesis, lipolysis

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Propionic acid and butyric acid inhibit lipolysis and de novo lipogenesis and increase insulin-stimulated glucose uptake in primary rat adipocytes

Cited by 94 publications

References 54 publications

Branched short-chain fatty acids modulate glucose and lipid metabolism in primary adipocytes

Branched short-chain fatty acids modulate glucose and lipid metabolism in primary adipocytes

Effects of gut microbiota manipulation onex vivolipolysis in human abdominal subcutaneous adipocytes

Arctigenin improves lipid metabolism by regulating AMP‐activated protein kinase and downstream signaling pathways

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