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Effect of Short-Chain Fatty Acids Produced by Probiotics
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Milena Fernandes da Silva, Meire dos Santos Falcão de Lima, Attilio Converti
There are several ways in which SCFAs protect the individual against obesity, via the activation of nutrient-specific receptors (Mulders et al. 2018). SCFAs’ affinity for the GPR41 receptor (Ffar3, free fatty acid receptor) depends on the organic acid chain length. Since the receptor GPR40, which is located near the GPR41 gene, binds to long chain fatty acids instead of SCFAs (Remely et al. 2014), it has been hypothesized that GPR41 might have no promoter region and be transcribed by the same GPR40 promoter (Bahar Halpern et al. 2012). These receptors are closely linked to the biological functions of lipid metabolism modulation, regulate the production of leptin and other hormones of satiety, and control the energy metabolism of the host (Mulders et al. 2018).
Sleep and Obesity Prevention in Children and Adolescents
Published in James M. Rippe, Lifestyle Medicine, 2019
Jill Lsbaugh Kaar, Stacey L. Simon
Children and adolescents with obesity are at increased risk for obstructive sleep apnea (OSA): the prevalence of OSA is approximately 1–5% in otherwise healthy children but increases to upward of 30% in children with obesity.63,64 OSA is characterized by repeated partial or total obstruction of the upper airway during the night, resulting in multiple arousals from sleep. Untreated, OSA can have severe negative consequences, including cardiovascular morbidity, cognitive deficits, and mood and behavior problems.64,65 Greater severity of OSA has been associated with adverse fat distribution, exercise function, and increased insulin resistance. In a study of 31 obese children age 5–18 years, visceral fat distribution assessed with MRI/MRS, was associated with OSA severity measured by PSG.66 Children with OSA ages 7–12 years, compared to weight-matched children without OSA, had lower cardiac output and oxygen consumption at peak exercise capacity independent of weight status.67 Despite similar levels of obesity, adolescent patients with moderate or severe OSA had higher fasting insulin and HOMA-IR compared to patients with mild or no OSA.68 Similarly, in a sample of 62 children ages 5–16 years referred for snoring, severity of OSA correlated with fasting insulin, independent of BMI.69 Gozal and colleagues70 conducted a study of 260 children ages 4–11 years and found that children with both obesity and OSA had the lowest levels of G protein-coupled receptor 120 (GPR 120), a long-chain free fatty acid receptor that plays a role in energy homeostasis and protects against insulin resistance and systemic inflammation, potentially contributing to food intake, weight, and glucose metabolism in youth with OSA. The extant studies are limited by the use of non-standard criteria for defining OSA and variable measurement of OSA, ranging from full polysomnography to parent report of symptoms. Future research is needed to further understand the role that OSA may play in relation to weight, exercise function, energy balance, and glucose metabolism.
Pathobionts: mechanisms of survival, expansion, and interaction with host with a focus on Clostridioides difficile
Published in Gut Microbes, 2021
Harish Chandra, Krishna Kant Sharma, Olli H. Tuovinen, Xingmin Sun, Pratyoosh Shukla
Fachi et al.47 demonstrated the role of microbiota-derived acetate in protection through the recruitment of neutrophils and ILC3s in acute mouse model of CDI. Acetate signals through free fatty acid receptor 2 on neutrophils and ILC3s and accelerates their recruitment to the site of infection. Acetate–FFAR2 interaction activated the inflammasome that resulted in the release of IL-1β and further promoted the secretion of IL-22 in ILC3 through IL-1 receptor signaling in response to IL-1β (Figure 2).47 In the mouse CDI model, secretion of IL-22 cytokine was induced and the IL-22-/- KO mice showed increased pathobiont load and resistance to complement mediated phagocytosis.105 Administration of IL-22 helped clear the pathobiont load by increased phagocytosis.
The role of short-chain fatty acids in the interplay between gut microbiota and diet in cardio-metabolic health
Published in Gut Microbes, 2021
Ana Nogal, Ana M. Valdes, Cristina Menni
SCFAs might present positive effects on body weight control by regulating the energy intake and energy expenditure. Some insights have been obtained into the mechanisms by which SCFAs regulate appetite. A potential mechanism might be the stimulation of secretion of gut-derived satiety hormones, such as peptide YY (PYY) and glucagon-like peptide 1 (GLP-1), by SCFAs binding to the free fatty acid receptor FFAR2 and FFAR3.124 Both hormones, which are secreted by intestinal enteroendocrine L-cells,125 influence appetite by activating proopiomelanocortin (POMC) neurons in the hypothalamic arcuate nucleus, suppressing neuropeptide Y (NPY), and delaying or inhibiting gastric emptying.126–128 Expression of genes encoding PYY is also regulated by receptor-independent pathways. Indeed, the inhibitory activity of HDAC by butyrate leads to an increased PYY expression in human L-cells.129 Besides, a study using in vivo11C-acetate and PET-CT acetate demonstrated that acetate can cross the blood-brain barrier and is taken up by the hypothalamus, causing an appetite decrease and increase of γ-aminobutyric acid and lactate.130 The secretion of leptin, which is often referred to as the “satiety hormone”, might be also stimulated by SCFAs, resulting in a decreased appetite.131,132 For instance, human adipocytes incubated with a high concentration of propionate appeared to increase the leptin mRNA expression and leptin secretion.133
Emerging therapeutic targets and preclinical models for severe asthma
Published in Expert Opinion on Therapeutic Targets, 2020
Izabela Galvão, Richard Y. Kim, Sijie Shen, Kurtis F. Budden, Angélica T. Vieira, Philip M. Hansbro
Acetate preferentially binds GPR43 (also known as free fatty acid receptor [FFAR]2), which is expressed by immune cells including neutrophils and eosinophils [123]. Gpr43/FFAR2-deficient mice have exaggerated inflammatory responses in the airways and lung tissue, compared to WT mice in Ova-induced AAD [124] and pneumonia [124,125]. Oral administration of the SCFA acetate and activation of these receptors is linked with initiating the resolution of inflammation in AAD [124]. Interestingly, recent evidence shows that activation of GPR43 increases alveolar macrophage killing activity and cytokine production in the lungs of mice infected with different pathogens, including RSV, Klebsiella pneumoniae, and Streptococcus pneumoniae [125,126]. Since lung infections are strongly associated with severe, steroid-resistant exacerbations of asthma, administration of acetate or Gpr43/FFA2 receptor agonists may be beneficial in severe asthma. However, the anti-inflammatory effects of SCFAs are not limited to GPR43, as acetate treatment protected against AAD even in mice deficient of GPR43 [127].