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Current Aspects of the Role of Autoantibodies Directed Against Appetite-Regulating Hormones and the Gut Microbiome in Eating Disorders.
Smitka, K, Prochazkova, P, Roubalova, R, Dvorak, J, Papezova, H, Hill, M, Pokorny, J, Kittnar, O, Bilej, M, Tlaskalova-Hogenova, H
Frontiers in endocrinology. 2021;:613983
Abstract
The equilibrium and reciprocal actions among appetite-stimulating (orexigenic) and appetite-suppressing (anorexigenic) signals synthesized in the gut, brain, microbiome and adipose tissue (AT), seems to play a pivotal role in the regulation of food intake and feeding behavior, anxiety, and depression. A dysregulation of mechanisms controlling the energy balance may result in eating disorders such as anorexia nervosa (AN) and bulimia nervosa (BN). AN is a psychiatric disease defined by chronic self-induced extreme dietary restriction leading to an extremely low body weight and adiposity. BN is defined as out-of-control binge eating, which is compensated by self-induced vomiting, fasting, or excessive exercise. Certain gut microbiota-related compounds, like bacterial chaperone protein Escherichia coli caseinolytic protease B (ClpB) and food-derived antigens were recently described to trigger the production of autoantibodies cross-reacting with appetite-regulating hormones and neurotransmitters. Gut microbiome may be a potential manipulator for AT and energy homeostasis. Thus, the regulation of appetite, emotion, mood, and nutritional status is also under the control of neuroimmunoendocrine mechanisms by secretion of autoantibodies directed against neuropeptides, neuroactive metabolites, and peptides. In AN and BN, altered cholinergic, dopaminergic, adrenergic, and serotonergic relays may lead to abnormal AT, gut, and brain hormone secretion. The present review summarizes updated knowledge regarding the gut dysbiosis, gut-barrier permeability, short-chain fatty acids (SCFA), fecal microbial transplantation (FMT), blood-brain barrier permeability, and autoantibodies within the ghrelin and melanocortin systems in eating disorders. We expect that the new knowledge may be used for the development of a novel preventive and therapeutic approach for treatment of AN and BN.
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The influence of fasting and energy-restricted diets on leptin and adiponectin levels in humans: A systematic review and meta-analysis.
Varkaneh Kord, H, M Tinsley, G, O Santos, H, Zand, H, Nazary, A, Fatahi, S, Mokhtari, Z, Salehi-Sahlabadi, A, Tan, SC, Rahmani, J, et al
Clinical nutrition (Edinburgh, Scotland). 2021;(4):1811-1821
Abstract
BACKGROUND & AIMS Fasting and energy-restricted diets have been evaluated in several studies as a means of improving cardiometabolic biomarkers related to body fat loss. However, further investigation is required to understand potential alterations of leptin and adiponectin concentrations. Thus, we performed a systematic review and meta-analysis to derive a more precise estimate of the influence of fasting and energy-restricted diets on leptin and adiponectin levels in humans, as well as to detect potential sources of heterogeneity in the available literature. METHODS A comprehensive systematic search was performed in Web of Science, PubMed/MEDLINE, Cochrane, SCOPUS and Embase from inception until June 2019. All clinical trials investigating the effects of fasting and energy-restricted diets on leptin and adiponectin in adults were included. RESULTS Twelve studies containing 17 arms and a total of 495 individuals (intervention = 249, control = 246) reported changes in serum leptin concentrations, and 10 studies containing 12 arms with a total of 438 individuals (intervention = 222, control = 216) reported changes in serum adiponectin concentrations. The combined effect sizes suggested a significant effect of fasting and energy-restricted diets on leptin concentrations (WMD: -3.690 ng/ml, 95% CI: -5.190, -2.190, p ≤ 0.001; I2 = 84.9%). However, no significant effect of fasting and energy-restricted diets on adiponectin concentrations was found (WMD: -159.520 ng/ml, 95% CI: -689.491, 370.451, p = 0.555; I2 = 74.2%). Stratified analyses showed that energy-restricted regimens significantly increased adiponectin (WMD: 554.129 ng/ml, 95% CI: 150.295, 957.964; I2 = 0.0%). In addition, subsequent subgroup analyses revealed that energy restriction, to ≤50% normal required daily energy intake, resulted in significantly reduced concentrations of leptin (WMD: -4.199 ng/ml, 95% CI: -7.279, -1.118; I2 = 83.9%) and significantly increased concentrations of adiponectin (WMD: 524.04 ng/ml, 95% CI: 115.618, 932.469: I2 = 0.0%). CONCLUSION Fasting and energy-restricted diets elicit significant reductions in serum leptin concentrations. Increases in adiponectin may also be observed when energy intake is ≤50% of normal requirements, although limited data preclude definitive conclusions on this point.
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Effectiveness of eight-week zinc supplementation on vitamin D3 status and leptin levels in a population of postmenopausal women: a double-blind randomized trial.
Vázquez-Lorente, H, Molina-López, J, Herrera-Quintana, L, Gamarra-Morales, Y, López-González, B, Planells, E
Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS). 2021;:126730
Abstract
BACKGROUND The menopausal period is characterized by hormonal imbalance related to the alteration of parameters involved in lipid metabolism. In addition, menopause increases the risk of deficiencies of key vitamins and minerals such as vitamin D and zinc in such women. The present study investigates the influence of zinc supplementation on the status of vitamin D3 and other lipid parameters in postmenopausal women. METHODS Fifty-one healthy postmenopausal women aged 44-76 years from the province of Granada (Spain) were divided into two groups (placebo and zinc) of 25 and 26 women, respectively. The zinc group was supplemented with 50 mg/day of zinc for 8 weeks. Nutrient intake assessment was performed by means of a 24 -h reminder. Zinc was determined by flame atomic absorption spectrophotometry. Vitamin D was analyzed by liquid chromatography - tandem mass spectrometry. Leptin was determined by enzyme immunoassay. RESULTS Zinc supplementation improved the initial vitamin D3 status of the postmenopausal population (p = 0.049). Plasma levels of 25-OH-D3 increased significantly after Zn supplementation in women with lower age at menopause (p = 0.045). Both intake and plasma zinc levels were inversely correlated to serum leptin levels (p = 0.044 and p = 0.033, respectively), being significantly lower in lower age at menopause (p < 0.001). CONCLUSION Zinc supplementation improved vitamin D3 status and was associated to low leptin levels in the postmenopausal women of the study.
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Effects of dehydroepiandrosterone (DHEA) supplementation on cortisol, leptin, adiponectin, and liver enzyme levels: A systematic review and meta-analysis of randomised clinical trials.
Chen, H, Jin, Z, Sun, C, Santos, HO, Kord Varkaneh, H
International journal of clinical practice. 2021;(11):e14698
Abstract
BACKGROUND AND AIMS Dehydroepiandrosterone (DHEA) supplementation has been investigated in patients with altered cortisol levels and is proposed to ameliorate the metabolic profile related to adipose tissue. However, further research is warranted and evidence is no compelling for liver safety. Hence, we aimed to meta-analyse the effects of DHEA supplementation on circulating levels of cortisol, liver enzymes, and adipokines. METHODS We searched literature published in PubMed, Web of Science, Embase and Scopus, until December 2020. We obtained overall results using the generic inverse of variance method with a random-effects model. RESULTS Through 10 arms, serum cortisol levels decreased significantly after DHEA supplementation [weighted mean difference (WMD): -53.581 nmol/L, 95% confidence interval (CI): -88.2, -18.9, P = .002], without significant heterogeneity (I2 = 36%, P = .117). In contrast, any significance was noted for adiponectin (WMD: -0.045 µg/mL, 95% CI: -0.56, 0.47; P = .865), leptin (WMD: -2.55 µg/mL, 95% CI: -6.2, 1.06; P = .166), aspartate transaminase (AST) (WMD: -3.7 U/L, 95% CI: -10.35, 2.95; P = .276), and alanine aminotransferase (ALT) (WMD: -1.7 U/L, 95% CI: -3.45, 0.06; P = .058). CONCLUSION DHEA supplementation decreased circulating cortisol but did not alter adiponectin, leptin, AST, and ALT levels. Hence, DHEA supplementation could be considered as an adjunct in the management of hypercortisolaemia and is safe for the liver.
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5.
Leptin as a Biomarker of Stress: A Systematic Review and Meta-Analysis.
Bouillon-Minois, JB, Trousselard, M, Thivel, D, Benson, AC, Schmidt, J, Moustafa, F, Bouvier, D, Dutheil, F
Nutrients. 2021;(10)
Abstract
BACKGROUND Leptin is a satiety hormone mainly produced by white adipose tissue. Decreasing levels have been described following acute stress. OBJECTIVE To conduct a systematic review and meta-analysis to determine if leptin can be a biomarker of stress, with levels decreasing following acute stress. METHODS PubMed, Cochrane Library, Embase, and ScienceDirect were searched to obtain all articles studying leptin levels after acute stress on 15 February 2021. We included articles reporting leptin levels before and after acute stress (physical or psychological) and conducted random effects meta-analysis (DerSimonian and Laird approach). We conducted Meta-regressions and sensitivity analyses after exclusion of groups outside the metafunnel. RESULTS We included seven articles-four cohort and three case-control studies-(28 groups) from 27,983 putative articles. Leptin levels decreased after the stress intervention (effect size = -0.34, 95%CI -0.66 to -0.02) compared with baseline levels, with a greater decrease after 60 min compared to mean decrease (-0.45, -0.89 to -0.01) and in normal weight compared to overweight individuals (-0.79, -1.38 to -0.21). There was no difference in the overweight population. Sensitivity analyses demonstrated similar results. Levels of leptin after stress decreased with sex ratio-i.e., number of men/women-(-0.924, 95%CI -1.58 to -0.27) and increased with the baseline levels of leptin (0.039, 0.01 to 0.07). CONCLUSIONS Leptin is a biomarker of stress, with a decrease following acute stress. Normal-weight individuals and women also have a higher variation of leptin levels after stress, suggesting that leptin may have implications in obesity development in response to stress in a sex-dependent manner.
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Adiponectin/leptin ratio increases after a 12-week very low-carbohydrate, high-fat diet, and exercise training in healthy individuals: A non-randomized, parallel design study.
Cipryan, L, Dostal, T, Plews, DJ, Hofmann, P, Laursen, PB
Nutrition research (New York, N.Y.). 2021;:22-30
Abstract
This study aimed to investigate the effect of a 12-week very low-carbohydrate, high-fat (VLCHF) diet and exercise on biomarkers of inflammation in healthy individuals. Since the anti-inflammatory effects of a ketogenic diet have been established, we hypothesized that the VLCHF diet, along with exercise, would have an additional favorable effect on biomarkers of inflammation. Twenty-four healthy individuals were allocated to the VLCHF diet (VLCHF N = 12, age 25.3 ± 2.0 years, body mass 66.7 ± 9.8 kg, fat mass 21.5% ± 4.9%), or habitual diet (HD: N = 12, age 23.9 ± 3.8 years, body mass 72.7 ± 15.0 kg, fat mass 23.4 ± 8.4 %) group. Biomarkers of inflammation (adiponectin, leptin, and high-sensitive interleukin-6 [hs-IL-6]) and substrate metabolism (glycated hemoglobin, fasting glucose, triacylglycerides, and cholesterol) were analyzed from blood at baseline and after 12 weeks. The adiponectin-leptin ratio significantly increased in the VLCHF group after the intervention period (ES [95% CL]: -0.90 [-0.96, -0.77], P ≤ .001, BF10 = 22.15). The adiponectin-leptin ratio changes were associated with both a significant increase in adiponectin (-0.79 [-0.91, -0.54], P ≤ .001, BF10 = 9.43) and a significant decrease in leptin (0.58 [0.19, 0.81], P = .014, BF10 = 2.70). There was moderate evidence of changes in total cholesterol (-1.15 [-2.01, -0.27], P = .010, BF10 = 5.20), and LDL cholesterol (-1.12 [-2.01, -0.21], P = .016, BF10 = 4.56) in the VLCHF group. Body weight (kg) and fat mass (%) decreased in the VLCHF group by 5.4% and 14.9%, respectively. We found that in healthy young individuals, consuming a VLCHF diet while performing regular exercise over a 12-week period produced favorable changes in body weight and fat mass along with beneficial changes in serum adiponectin and leptin concentrations. These data support the use of a VLCHF diet strategy for the primary prevention of chronic diseases associated with systemic low-grade inflammation.
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Effect of Dietary Fiber on Serum Leptin Level: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.
Hassanzadeh-Rostami, Z, Faghih, S
Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association. 2021;(4):322-333
Abstract
BACKGROUND Dietary fibers may induce satiety through affecting gastro-intestinal and peripheral appetite regulating hormones. Thus, we aimed to investigate the effect of dietary fiber consumption on serum leptin level compared to control diet, in short- and long- term trials, through a systematic review and meta-analysis. METHODS We searched PubMed, web of science, Scopus, ProQuest, EMBASE, and Cochrane Library to find randomized controlled clinical trials that evaluated effect of any type of dietary fiber on serum leptin level compared to control diet, until April 2019. Both short-term (1-4 days) and long-term (longer than 2 weeks) studies were selected. Mean differences (MD) of changes in serum leptin level and 95% confidence intervals were extracted from eligible studies, and random effects model was used to analyze data. RESULTS Thirteen studies included the systematic review and 11 entered in the meta-analysis. No significant change was seen in serum leptin level in short-term (MD=0.02, 95% CI; -0.15, 0.20, Tau2=0.0) and long-term studies (MD=-0.10, 95% CI; -0.28, 0.08, Tau2=0.0), followed by fiber consumption. However, this effect was statistically significant in obese participants (MD=-0.36, 95% CI; -0.71, -0.02, Tau2=0.0) in long-term studies. Moreover, we found no significant results in subgroups of baseline serum leptin level, intervention duration, fiber dose, and fiber type. CONCLUSIONS This meta-analysis found that taking dietary fiber for long term could lower serum leptin level, just in obese persons. However, further clinical trials are needed in this field to clarify this issue.
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Leptin brain entry via a tanycytic LepR-EGFR shuttle controls lipid metabolism and pancreas function.
Duquenne, M, Folgueira, C, Bourouh, C, Millet, M, Silva, A, Clasadonte, J, Imbernon, M, Fernandois, D, Martinez-Corral, I, Kusumakshi, S, et al
Nature metabolism. 2021;(8):1071-1090
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Abstract
Metabolic health depends on the brain's ability to control food intake and nutrient use versus storage, processes that require peripheral signals such as the adipocyte-derived hormone, leptin, to cross brain barriers and mobilize regulatory circuits. We have previously shown that hypothalamic tanycytes shuttle leptin into the brain to reach target neurons. Here, using multiple complementary models, we show that tanycytes express functional leptin receptor (LepR), respond to leptin by triggering Ca2+ waves and target protein phosphorylation, and that their transcytotic transport of leptin requires the activation of a LepR-EGFR complex by leptin and EGF sequentially. Selective deletion of LepR in tanycytes blocks leptin entry into the brain, inducing not only increased food intake and lipogenesis but also glucose intolerance through attenuated insulin secretion by pancreatic β-cells, possibly via altered sympathetic nervous tone. Tanycytic LepRb-EGFR-mediated transport of leptin could thus be crucial to the pathophysiology of diabetes in addition to obesity, with therapeutic implications.
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A carbohydrate-restricted diet for patients with irritable bowel syndrome lowers serum C-peptide, insulin, and leptin without any correlation with symptom reduction.
Saidi, K, Nilholm, C, Roth, B, Ohlsson, B
Nutrition research (New York, N.Y.). 2021;:23-36
Abstract
Alterations in gut endocrine cells and hormone levels have been measured in patients with irritable bowel syndrome (IBS). The hypothesis of the present study was that hormone levels would change after 4 weeks of a starch- and sucrose-reduced diet (SSRD) intervention corresponding to decreased carbohydrate intake and symptoms. Among 105 IBS patients from primary and tertiary healthcare, 80 were randomized to SSRD, while 25 followed their ordinary diet. Food diaries, Rome IV, and IBS-symptom severity score (IBS-SSS) questionnaires were completed, and blood samples were collected at baseline and after the intervention. Serum C-peptide, gastric inhibitory peptide, glucagon, glucagon-like peptide-1, insulin, leptin, luteinizing hormone, polypeptide YY, and glucose were measured, along with the prevalence of autoantibodies against gonadotropin-releasing hormone; its precursor, progonadoliberin-2, and receptor; and tenascin C. Carbohydrate intake was lower in the intervention group than in controls at week 4 (median: 88 [66-128] g vs 182 [89-224] g; P < .001). The change in carbohydrate intake, adjusted for weight, was associated with a decrease in C-peptide (β: 14.43; 95% confidence interval [CI]: 4.12-24.75) and insulin (β: 0.18; 95% CI: 0.04-0.32) levels. Glucose levels remained unchanged. The IBS-SSS scores were lower in the intervention group but not in controls (P < .001), without any association with changes in hormone concentrations. There was no difference in autoantibody prevalence between patients and healthy controls. In conclusion, the hypothesis that reduced carbohydrate intake corresponded to altered hormonal levels in IBS was accepted; however, there was no relationship between hormonal concentrations and symptoms.
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Efficacy and Safety of Lactobacillus plantarum K50 on Lipids in Koreans With Obesity: A Randomized, Double-Blind Controlled Clinical Trial.
Sohn, M, Na, GY, Chu, J, Joung, H, Kim, BK, Lim, S
Frontiers in endocrinology. 2021;:790046
Abstract
BACKGROUND Only few studies have investigated the role of probiotics in the development of obesity. We aimed to determine the efficacy and safety of an intake of Lactobacillus plantarum K50 (LPK) on body fat and lipid profiles in people with obesity. METHODS This randomized, double-blind, placebo-controlled, clinical trial involved 81 adults with a body mass index of 25-30 kg/m2 who were assigned randomly to a diet including 4 × 109 colony-forming unit of LPK or a placebo. Changes in body fat, anthropometric parameters, and biomarkers of obesity were compared using a linear mixed-effect model. RESULTS After 12 weeks of treatment, body weight, fat mass, and abdominal fat area did not change significantly in the two groups. However, total cholesterol levels decreased from 209.4 ± 34.4 mg/dL to 203.5 ± 30.9 mg/dL in the LPK group, but increased from 194.7 ± 37.5 mg/dL to 199.9 ± 30.7 mg/dL in the placebo group (P = 0.037). Similarly, triglyceride levels decreased from 135.4 ± 115.8 mg/dL to 114.5 ± 65.9 mg/dL in the LPK group, with a significant difference between groups. LPK supplementation also tended to decrease leptin levels compared with placebo. It also changed the distribution of gut microbiota significantly, with an increase in L. plantarum and a decrease in Actinobacteria, both of whose changes in abundance were correlated with changes in visceral adiposity, with borderline significance. CONCLUSION A 12-week consumption of LPK reduced the total cholesterol and triglyceride levels significantly with favorable alterations in microbiota, suggesting potential benefits for controlling blood lipid profiles.