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Nanotechnology and Probiotics
Published in Devarajan Thangadurai, Saher Islam, Jeyabalan Sangeetha, Natália Cruz-Martins, Biogenic Nanomaterials, 2023
Francine Schütz, Sofia Pinheiro, Rita Oliveira, Pedro Barata
To what concerns to metabolic disorders, probiotic intervention has also shown useful in obesity, with gut microbiota modulation resulting in lower insulin resistance and increased satiety, and as a consequence in a decrease in fat mass and body weight (Ejtaheda et al., 2019; Mazloom et al., 2019). In the colon, probiotics can also increase glucagon like peptide 2 (GLP-2) production with a higher expression of zonula occludens-1, recovery of the tight junction between epithelial cells and reduced gut permeability (Cani et al., 2009). Furthermore, the supplementation with some probiotics can increase the secretion of GLP-1 and peptide YY (PYY) by the gut, thus affecting insulin resistance and beta-cell function (Molinaro et al., 2012).
In vitro fermentation assay on the bifidogenic effect of steviol glycosides of Stevia rebaudiana plant for the development of dietetic novel products
Published in Preparative Biochemistry & Biotechnology, 2023
It has been proven that the intestinal microbiota and the type of nutrients taken are beneficial to the host in terms of metabolism. Butyric acid from SCFAs is effective as a primary food source for colon bacteria and also as a histone deacetylase inhibitor.[58] This fatty acid contributes to the maintenance of barrier integrity and reduces intestinal inflammation.[59,60] Acetic acid, propionic acid and butyric acid regulate key metabolic hormones including peptide YY (PYY) and GLP-1 (12, 23), activating G-protein-coupled receptors (GPRs) .[61,62] It has been found in studies that the formation of propionic acid, butyric acid or other SCFAs can improve insulin sensitivity and reduce obesity.[63]
Eating behaviours related to psychological stress are associated with functional hypothalamic amenorrhoea in exercising women
Published in Journal of Sports Sciences, 2020
Nicole C.A. Strock, Mary Jane De Souza, Nancy I. Williams
Much of the FHA literature in exercising women support a metabolic aetiology as the driving force for reproduction dysfunction. Prolonged energy deficiency prompts physiological adaptations, as the body redirects available metabolic fuels towards the physiological processes essential for survival, i.e., locomotion, cellular maintenance, and thermoregulation, while simultaneously suppressing growth and reproduction (Schneider & Wade, 1990, 1989; Wade et al., 1996). In an energy deficient state, suppressed hypothalamic-pituitary-thyroid signalling can be indicated by reduced thyroxine (T4), total triiodothyronine (T3) (MJ De Souza et al., 2008; Loucks et al., 1992), and the peripheral conversion of T4 to T3 (Agnihothri et al., 2014), ultimately leading to a reduced metabolic rate (RMR) (Koehler et al., 2016; Myerson et al., 1991). Other indications of downstream physiologic disruption are reflected in altered LH pulsatility (Loucks & Thuma, 2003; Loucks et al., 1985), reduced insulin-like growth factor-1 (IGF-1) (Kaufman et al., 2002), and uncoupled bone turnover (MJ De Souza et al., 2008; Ihle & Loucks, 2004). Appetite-regulating hormones involved in energy homoeostasis are also altered with energy deficiency, as fasting concentrations of peptide YY (PYY) and ghrelin remain elevated in exercising women with FHA (MJ De Souza et al., 2004; Scheid et al., 2009) and anorexic women (Misra et al., 2006). Importantly, evidence exists in both human (Williams et al., 2015) and animal studies (Williams, Caston-Balderrama et al., 2001; Williams, Helmreich et al., 2001), proving that energy deficiency is a causal factor in the induction of FHA.
Guided dietary fibre intake as a means of directing short-chain fatty acid production by the gut microbiota
Published in Journal of the Royal Society of New Zealand, 2020
Through liver gluconeogenesis, propionate is an important source of glucose for ruminants: as much as 90% of glucose in adult ruminants is derived by this method (Nafikov and Beitz 2007). Ruminant studies also showed a marked decrease in appetite following intravenous infusion with propionate (Bergman 1990; Farningham and White 1993; Arora et al. 2011). A liver-brain axis mechanism was suggested because blockading the vagus nerve close to the liver prevented the propionate-induced hypophagia (Anil and Forbes 1980). Propionate probably has much less importance as a source of glucose in humans than in ruminants (Morrison and Preston 2016). However, delivery of propionate directly to the human colon in the form of inulin-propionate ester resulted in increased release of anorectic gut hormones (peptide YY [PYY] and glucagon-like peptide 1 [GLP-1]) and reduced energy intake by the participants by about 14% (Chambers et al. 2015). The use of inulin-propionate ester ensured delivery of most of the propionate to the colon where the propionate was released by bacterial action. Long-term (24 weeks) delivery prevented further weight gain and reduced intra-abdominal fat accretion in overweight participants (Chambers et al. 2015). In rodents, GLP-1 release is due to stimulation of GPR43 (FFAR2) on endocrine cells in the gut mucosa (L cells) (Tolhurst et al. 2012). Administration of PYY or GLP-1 to humans enhances satiety and reduces food intake (Turton et al. 1996; Batterham et al. 2003). Using a similar approach in another human study, functional NMR showed reductions in blood oxygen level-dependent signals in brain regions associated with reward processing during food picture testing (Byrne et al. 2016). The participants also had reduced energy intake during an ad libitum meal. These changes, however, were independent of plasma PYY and GLP-1 levels (Byrne et al. 2016). Adverse influences of calcium propionate (used in bread as a preservative) ingested with food by mice (glycogenolysis, hyperglycaemia) are unlikely to be relevant in the context of dietary fibre (Tirosh et al. 2019); the propionate in food is quickly absorbed in the small bowel whereas in situ production by the microbiota leads to binding to colonic receptors.