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Effects of Diets on Adipose Tissue.
Ezquerro, S, Rodríguez, A, Portincasa, P, Frühbeck, G
Current medicinal chemistry. 2019;(19):3593-3612
Abstract
BACKGROUND Obesity is a major health problem that has become a global epidemic. Overweight and obesity are commonly associated with the development of several pathologies, such as insulin resistance, cardiovascular diseases, sleep apnea and several types of cancer, which can lead to further morbidity and mortality. An increased abdominal adiposity renders overweight and obese individuals more prone to metabolic and cardiovascular problems. OBJECTIVE This Review aims to describe the dietary strategies to deal with excess adiposity given the medical, social and economic consequences of obesity. METHODS One hundred and eighty-five papers were included in the present Review. RESULTS Excess adiposity leads to several changes in the biology, morphology and function of the adipose tissue, such as adipocyte hypertrophy and hyperplasia, adipose tissue inflammation and fibrosis and an impaired secretion of adipokines, contributing to the onset of obesity- related comorbidities. The first approach for obesity management and prevention is the implementation of a diet combined with physical activity. The present review summarizes the compelling evidence showing body composition changes, impact on cardiometabolism and potential adverse effects of very-low calorie, low- and high-carbohydrate, high-protein or low-fat diets. The use of macronutrients during the preprandial and postprandial state has been also reviewed to better understand the metabolic changes induced by different dietary interventions. CONCLUSION Dietary changes should be individualised, tailored to food preferences and allow for flexible approaches to reducing calorie intake in order to increase the motivation and compliance of overweight and obese patients.
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The Effect of Low Glycemic Index and Glycemic Load Diets on Hepatic Fat Mass, Insulin Resistance, and Blood Lipid Panels in Individuals with Nonalcoholic Fatty Liver Disease.
Parker, A, Kim, Y
Metabolic syndrome and related disorders. 2019;(8):389-396
Abstract
Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease that is associated with insulin resistance and hepatic triglyceride accumulation. There is evidence to suggest that a low glycemic index (GI) diet can reduce glucose absorption, hepatic influx of glucose, and de novo lipogenesis. This review investigates the effect of low GI and glycemic load (GL) diets on hepatic fat mass, hepatic enzymes, insulin resistance, fasting blood glucose levels, and blood lipid panels in individuals with NAFLD. PubMed, Cumulative Index to Nursing and Allied Health Literature, and Web of Science were used in literature search. Search keywords included "glycemic index," "glycaemic index," "glycemic load," "glycaemic load," "nonalcoholic fatty liver disease," "NAFLD," "nonalcoholic steatohepatitis," and "NASH." Outcome measurements included hepatic fat mass, hepatic enzyme alanine transaminase (ALT), insulin resistance [homeostasis model assessment of insulin resistance (HOMA-IR)], fasting blood glucose levels, and/or blood lipid panels. Four eligible studies enrolling 281 individuals with NAFLD were included. Both hepatic fat mass and ALT showed significant reductions from baseline in both low GI and GL diets. One study showed no change, and another study showed significant reductions in HOMA-IR. No significant reduction in fasting blood glucose level, triglycerides, high-density lipoprotein-cholesterol, or low-density lipoprotein-cholesterol was observed from baseline in both low GI and GL diets. Findings from the review suggest that low GI and GL diets may reduce hepatic fat mass and ALT in individuals with NAFLD. Future research of large-scale, randomized controlled studies using isoenergetic, low GI and GL diets for long term is needed to draw conclusionary results.
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Adipokines, adiposity, and bone marrow adipocytes: Dangerous accomplices in multiple myeloma.
Morris, EV, Edwards, CM
Journal of cellular physiology. 2018;(12):9159-9166
Abstract
Obesity has become a global epidemic influencing the establishment and progression of a wide range of diseases, such as diabetes, cardiovascular disease, and cancer. In 2016, International Agency for Research on Cancer reported that obesity is now associated with 13 different cancers, one of which is multiple myeloma (MM), a destructive cancer of plasma cells that predominantly reside in the bone marrow. Obesity is the accumulation of excess body fat, which causes metabolic, endocrine, immunologic, and inflammatory-like changes. Obesity is usually associated with an increase in visceral and/or subcutaneous fat; however, an additional fat depot that also responds to diet-induced changes is bone marrow adipose tissue (BMAT). There have been several studies over the past few decades that have identified BMAT as a key driver in MM progression. Adipocytes secrete numerous adipokines, such as leptin, adiponectin, resistin, adipsin, and visfatin, which when secreted at normal controlled levels have protective properties. However, in obesity these levels of secretion change, coupled with an increase in adipocyte number and size causing a profound and lasting effect on the bone microenvironment, contributing to MM cell growth, survival, and migration as well as potentially fueling bone destruction. Obesity is a modifiable risk factor making it an attractive option for targeted therapy. This review discusses the link between obesity, monoclonal gammopathy of undetermined significance (a benign condition that precedes MM), and myeloma, and the contribution of key adipokines to disease establishment and progression.
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Effect of pasta in the context of low-glycaemic index dietary patterns on body weight and markers of adiposity: a systematic review and meta-analysis of randomised controlled trials in adults.
Chiavaroli, L, Kendall, CWC, Braunstein, CR, Blanco Mejia, S, Leiter, LA, Jenkins, DJA, Sievenpiper, JL
BMJ open. 2018;(3):e019438
Abstract
OBJECTIVE Carbohydrate staples such as pasta have been implicated in the obesity epidemic. It is unclear whether pasta contributes to weight gain or like other low-glycaemic index (GI) foods contributes to weight loss. We synthesised the evidence of the effect of pasta on measures of adiposity. DESIGN Systematic review and meta-analysis using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. DATA SOURCES MEDLINE, Embase, CINAHL and the Cochrane Library were searched through 7 February 2017. ELIGIBILITY CRITERIA FOR SELECTING STUDIES We included randomised controlled trials ≥3 weeks assessing the effect of pasta alone or in the context of low-GI dietary patterns on measures of global (body weight, body mass index (BMI), body fat) and regional (waist circumference (WC), waist-to-hip ratio (WHR), sagittal abdominal diameter (SAD)) adiposity in adults. DATA EXTRACTION AND SYNTHESIS Two independent reviewers extracted data and assessed risk of bias. Data were pooled using the generic inverse-variance method and expressed as mean differences (MDs) with 95% CIs. Heterogeneity was assessed (Cochran Q statistic) and quantified (I2 statistic). GRADE assessed the certainty of the evidence. RESULTS We identified no trial comparisons of the effect of pasta alone and 32 trial comparisons (n=2448 participants) of the effect of pasta in the context of low-GI dietary patterns. Pasta in the context of low-GI dietary patterns significantly reduced body weight (MD=-0.63 kg; 95% CI -0.84 to -0.42 kg) and BMI (MD=-0.26 kg/m2; 95% CI -0.36 to -0.16 kg/m2) compared with higher-GI dietary patterns. There was no effect on other measures of adiposity. The certainty of the evidence was graded as moderate for body weight, BMI, WHR and SAD and low for WC and body fat. CONCLUSIONS Pasta in the context of low-GI dietary patterns does not adversely affect adiposity and even reduces body weight and BMI compared with higher-GI dietary patterns. Future trials should assess the effect of pasta in the context of other 'healthy' dietary patterns. TRIAL REGISTRATION NUMBER NCT02961088; Results.
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Sleep, Health, and Metabolism in Midlife Women and Menopause: Food for Thought.
Kravitz, HM, Kazlauskaite, R, Joffe, H
Obstetrics and gynecology clinics of North America. 2018;(4):679-694
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Abstract
Sleep and metabolism are essential components of health. Metabolic health depends largely on individual's lifestyle. Disturbances in sleep health, such as changes in sleep patterns that are associated with menopause/reproductive aging and chronologic aging, may have metabolic health consequences. Sleep restriction and age-related changes in sleep and circadian rhythms may influence changes in appetite and reproductive hormones, energy expenditure, and body adiposity. In this article, the authors describe how menopause-related sleep disturbance may affect eating behavior patterns, immunometabolism, immunometabolic dysfunction, and associations between sleep and metabolic outcomes.
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Adiposity and gastrointestinal cancers: epidemiology, mechanisms and future directions.
Murphy, N, Jenab, M, Gunter, MJ
Nature reviews. Gastroenterology & hepatology. 2018;(11):659-670
Abstract
Excess adiposity is a risk factor for several cancers of the gastrointestinal system, specifically oesophageal adenocarcinoma and colorectal, small intestine, pancreatic, liver, gallbladder and stomach cancers. With the increasing prevalence of obesity in nearly all regions of the world, this relationship could represent a growing source of cancers of the digestive system. Experimental and molecular epidemiological studies indicate important roles for alterations in insulin signalling, adipose tissue-derived inflammation and sex hormone pathways in mediating the association between adiposity and gastrointestinal cancer. The intestinal microbiome, gut hormones and non alcoholic fatty liver disease (NAFLD) also have possible roles. However, important gaps remain in our knowledge. For instance, our understanding of how adiposity throughout the life course is related to the risk of gastrointestinal cancer development and of how obesity influences gastrointestinal cancer prognosis and survival is limited. Nonetheless, the increasing use of state-of-the-art analytical methods (such as omics technologies, Mendelian randomization and MRI) in large-scale epidemiological studies offers exciting opportunities to advance our understanding of the complex relationship between adiposity and gastrointestinal cancers. Here, we examine the epidemiology of associations between obesity and gastrointestinal cancer, explore potential mechanisms underlying these relationships and highlight important unanswered research questions.
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From inflammation to sexual dysfunctions: a journey through diabetes, obesity, and metabolic syndrome.
Maiorino, MI, Bellastella, G, Giugliano, D, Esposito, K
Journal of endocrinological investigation. 2018;(11):1249-1258
Abstract
Metabolic diseases are associated with chronic low-grade inflammation, which has been indicated as a potential mediator of endothelial dysfunction and cardiovascular disease. Visceral adiposity is thought to be the starting condition of the inflammatory state through the release of inflammatory cytokines, including TNF-alpha, CRP, and IL-6, which in turn promote endothelial dysfunction, endothelial expression of chemokines (IL-1) and adhesion molecules (ICAM-1, VCAM-1, and P-selectin), and the inhibition of anti-atherogenic factors (adiponectin). Obesity, metabolic diseases, and diabetes, all conditions characterized by abdominal fat, are well-recognized risk factors for sexual dysfunction in both sexes. Evidence from randomized-controlled trials supports the association between inflammatory milieau and erectile dysfunction in men suffering from metabolic diseases, whereas, in women, this has to be confirmed in further studies. A healthy lifestyle based on dietary pattern with high content of whole grain, fruit, nuts and seeds, and vegetables and low in sodium and saturated fatty acids plus regular physical activity may help to modulate the pro-inflammatory state associated with metabolic diseases and the related burden of sexual dysfunctions.
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Adiposity, vitamin D requirements, and clinical implications for obesity-related metabolic abnormalities.
Hyppönen, E, Boucher, BJ
Nutrition reviews. 2018;(9):678-692
Abstract
This review was conducted to clarify both the complex interrelationship between adiposity and vitamin D and the clinical implications of vitamin D status on metabolic abnormalities associated with obesity. Obesity increases the risk of vitamin D deficiency, a finding consistently reported across all ages and in different population groups. According to genetic studies, this is driven by the effect of higher adiposity, which causes a reduction in circulating concentrations of 25-hydroxyvitamin D [25(OH)D, used as an indicator of vitamin D status]. Conversely, higher concentrations of 25(OH)D do not appear to affect the risk of obesity. Evidence from clinical trials using vitamin D supplementation to achieve weight reduction is limited. Some trials, however, have suggested that concomitant supplementation with vitamin D and calcium potentially reduces central fat deposits, especially in individuals with low dietary calcium intakes. Adiposity has important implications for the efficacy of vitamin D supplementation, and increases in 25(OH)D concentrations are generally lower in obese than in normal-weight individuals. Active hormonal vitamin D has many mechanistic effects, both physiologically and biochemically, that could counteract the harmful effects of obesity on metabolism and reduce the risks of metabolic abnormalities and tissue damage consequent to adiposity. Whether improvements in the overall obesogenic metabolic profile can be achieved by vitamin D supplementation, however, is still unknown.
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Adiposity, breast density, and breast cancer risk: epidemiological and biological considerations.
Soguel, L, Durocher, F, Tchernof, A, Diorio, C
European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP). 2017;(6):511-520
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Abstract
Excess total body fat and abdominal adipose tissue are recognized risk factors for metabolic diseases but also for some types of cancers, including breast cancer. Several biological mechanisms in connection with local and systemic effects of adiposity are believed to be implicated in breast cancer development, and may involve breast fat. Breast adipose tissue can be studied through mammography by looking at breast density features such as the nondense area mainly composed of fat, or the percent breast density, which is the proportion of fibroglandular tissue in relation to fat. The relation between adiposity, breast density features, and breast cancer is complex. Studies suggest a paradoxical association as adiposity and absolute nondense area correlate positively with each other, but in contrast to adiposity, absolute nondense area seems to be associated negatively with breast cancer risk. As breast density is one of the strongest risk factors for breast cancer, it is therefore critical to understand how these factors interrelate. In this review, we discuss these relations by first presenting how adiposity measurements and breast density features are linked to breast cancer risk. Then, we used a systematic approach to capture the literature to review the relation between adiposity and breast density features. Finally, the role of adipose tissue in carcinogenesis is discussed briefly from a biological perspective.
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Fruit consumption and adiposity status in adults: A systematic review of current evidence.
Hebden, L, O'Leary, F, Rangan, A, Singgih Lie, E, Hirani, V, Allman-Farinelli, M
Critical reviews in food science and nutrition. 2017;(12):2526-2540
Abstract
The aim of this review was to update current understanding of the potential association between fruit consumption and adiposity status in adult populations. Electronic databases were searched from January 1, 1997 to the search date of August 15, 2014, retrieving 4382 abstracts that were reviewed for eligibility: randomized controlled trial (RCT) or prospective cohort (PC), published in English, assessing the effect of whole fruit or fruit juice consumption on adiposity in healthy adult populations. Quality ratings for the 11 included RCTs were either positive (n = 2), neutral (n = 8), or negative (n = 1), while the six included PCs were either positive (n = 4) or neutral (n = 2). Consumption of whole fruit was found to contribute to a reduced risk for long-term weight gain in middle-aged adults. Experimental trials suggest this beneficial effect of whole fruit is mediated by a reduction in total energy intake. Fruit juice, however, had an opposing effect, promoting weight gain over the long term. This review reinforces national food-based dietary guidelines, encouraging the consumption of whole fruits and replacing fruit juices with plain water, as part of a broader set of dietary strategies to reduce total dietary energy intake in adult populations.