1.
Ghrelin forms in the modulation of energy balance and metabolism.
Gortan Cappellari, G, Barazzoni, R
Eating and weight disorders : EWD. 2019;(6):997-1013
Abstract
Ghrelin is a gastric hormone circulating in acylated (AG) and unacylated (UnAG) forms. This narrative review aims at presenting current emerging knowledge on the impact of ghrelin forms on energy balance and metabolism. AG represents ~ 10% of total plasma ghrelin, has an appetite-stimulating effect and is the only form for which a receptor has been identified. Moreover, other metabolic AG-induced effects have been reported, including the modulation of glucose homeostasis with stimulation of liver gluconeogenesis, the increase of fat mass and the improvement of skeletal muscle mitochondrial function. On the other hand, UnAG has no orexigenic effects, however recent reports have shown that it is directly involved in the modulation of skeletal muscle energy metabolism by improving a cluster of interlinked functions including mitochondrial redox activities, tissue inflammation and insulin signalling and action. These findings are in agreement with human studies which show that UnAG circulating levels are positively associated with insulin sensitivity both in metabolic syndrome patients and in a large cohort from the general population. Moreover, ghrelin acylation is regulated by a nutrient sensor mechanism, specifically set on fatty acids availability. These recent findings consistently point towards a novel independent role of UnAG as a regulator of muscle metabolic pathways maintaining energy status and tissue anabolism. While a specific receptor for UnAG still needs to be identified, recent evidence strongly supports the hypothesis that the modulation of ghrelin-related molecular pathways, including those involved in its acylation, may be a potential novel target in the treatment of metabolic derangements in disease states characterized by metabolic and nutritional complications.Level of evidence Level V, narrative review.
2.
The Effects of Synbiotic Supplementation on Body Mass Index, Metabolic and Inflammatory Biomarkers, and Appetite in Patients with Metabolic Syndrome: A Triple-Blind Randomized Controlled Trial.
Rabiei, S, Hedayati, M, Rashidkhani, B, Saadat, N, Shakerhossini, R
Journal of dietary supplements. 2019;(3):294-306
Abstract
It has been shown recently that metabolic syndrome is associated with gut dysbiosis. The gut microbiota may be the main target for prevention or treatment of metabolic syndrome. We investigated the effects of synbiotic supplementation on metabolic syndrome. In this triple-blinded clinical trial, 46 Iranian patients with metabolic syndrome, from both sexes, aged 25-70 years, who fulfilled inclusion criteria were randomly categorized to receive either the synbiotic or a placebo capsule, twice a day for three months, plus a weight-loss diet using stratified random sampling based on body mass index (BMI). Each synbiotic capsule consisted of seven strains probiotic bacteria (2× 108) plus fructooligosaccharide as a prebiotic. Anthropometric measurements and biochemical tests were assessed at baseline and at the end of week 12 for fasting blood sugar (FBS), insulin, lipid profile, high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), peptide YY (PYY), and glucagon-like peptide-1 (GLP-1). The mean changes of weight, BMI, FBS, insulin, homeostatic model assessment for insulin resistance (HOMA-IR), and GLP-1 between the two groups was statistically significant (p < .001). Furthermore, peptide YY (PYY) increased significantly in the synbiotic group (p ≤ .05). The trend of weight loss in the synbiotic group was significant until the end of the study (p < .001) while it stopped at week 6 in the placebo group. Synbiotic treatment may improve the status of BMI, FBS, insulin resistance, HOMA-IR, GLP-1, and PYY in patients with metabolic syndrome.
3.
Mechanisms of obesity in Prader-Willi syndrome.
Khan, MJ, Gerasimidis, K, Edwards, CA, Shaikh, MG
Pediatric obesity. 2018;(1):3-13
Abstract
Obesity is the most common cause of metabolic complications and poor quality of life in Prader-Willi syndrome (PWS). Hyperphagia and obesity develop after an initial phase of poor feeding and failure to thrive. Several mechanisms for the aetiology of obesity in PWS are proposed, which include disruption in hypothalamic pathways of satiety control resulting in hyperphagia, aberration in hormones regulating food intake, reduced energy expenditure because of hypotonia and altered behaviour with features of autism spectrum disorder. Profound muscular hypotonia prevents PWS patients from becoming physically active, causing reduced muscle movements and hence reduced energy expenditure. In a quest for the aetiology of obesity, recent evidence has focused on several appetite-regulating hormones, growth hormone, thyroid hormones and plasma adipocytokines. However, despite advancement in understanding of the genetic basis of PWS, there are contradictory data on the role of satiety hormones in hyperphagia and data regarding dietary intake are limited. Mechanistic studies on the aetiology of obesity and its relationship with disease pathogenesis in PWS are required. . In this review, we focused on the available evidence regarding mechanisms of obesity and potential new areas that could be explored to help unravel obesity pathogenesis in PWS.