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1.
Determinants of ectopic liver fat in metabolic disease.
Bosy-Westphal, A, Braun, W, Albrecht, V, Müller, MJ
European journal of clinical nutrition. 2019;(2):209-214
Abstract
Common obesity-associated hepatic steatosis (nonalcoholic fatty liver disease (NAFLD)) and insulin resistance are mainly caused by dysfunctional adipose tissue. This adipose tissue dysfunction leads to increased delivery of NEFA and glycerol to the liver that (i) drives hepatic gluconeogenesis and (ii) facilitates the accumulation of lipids and insulin signaling inhibiting lipid intermediates. Dysfunctional adipose tissue can be caused by impaired lipid storage (overflow hypothesis, characterized by large visceral adipocytes) or increased lipolysis (due to impaired postprandial suppression of lipolysis in inflamed, insulin-resistant adipocytes). In line with the adipose tissue expandability hypothesis the amount and distribution of adipose tissue correlate with its dysfunction and thus with liver fat. This relationship is however modified by endocrine effects on lipid storage and lipolysis as well as dietary effects on hepatic lipogenesis and lipid oxidation. The association between body composition characteristics like visceral obesity or fat cell size and ectopic liver fat is modified by these influences. Phenotyping obesity according to metabolic risk should integrate body composition characteristics, endocrine parameters and information on diet.
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2.
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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3.
Macronutrients and the Adipose-Liver Axis in Obesity and Fatty Liver.
Duwaerts, CC, Maher, JJ
Cellular and molecular gastroenterology and hepatology. 2019;(4):749-761
Abstract
Macronutrient metabolism is a highly orchestrated process, with adipose tissue and liver each playing central roles in nutrient uptake, processing, transport, and storage. These 2 tissues form an important metabolic circuit, particularly as it relates to lipids as the primary storage form of excess energy. The function of the circuit is influenced by many factors, including the quantity and type of nutrients consumed and their impact on the overall health of the tissues. In this review we begin with a brief summary of the homeostatic disposition of lipids between adipose tissue and liver and how these processes can become dysregulated in obesity. We then explore how specific dietary nutrients and nutrient combinations can exert unique influences on the liver-adipose tissue axis.
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4.
Adipose Tissue Quality in Aging: How Structural and Functional Aspects of Adipose Tissue Impact Skeletal Muscle Quality.
De Carvalho, FG, Justice, JN, Freitas, EC, Kershaw, EE, Sparks, LM
Nutrients. 2019;(11)
Abstract
The interplay between adipose tissue and skeletal muscle and the impact on mobility and aging remain enigmatic. The progressive decline in mobility promoted by aging has been previously attributed to the loss of skeletal mass and function and more recently linked to changes in body fat composition and quantity. Regardless of body size, visceral and intermuscular adipose depots increase with aging and are associated with adverse health outcomes. However, the quality of adipose tissue, in particular abdominal subcutaneous as it is the largest depot, likely plays a significant role in aging outcomes, such as mobility decline, though its communication with other tissues such as skeletal muscle. In this review, we discuss the age-associated development of a pro-inflammatory profile, cellular senescence, and metabolic inflexibility in abdominal subcutaneous adipose tissue. Collectively, these facets of adipose tissue quality influence its secretory profile and crosstalk with skeletal muscle and likely contribute to the development of muscle atrophy and disability. Therefore, the identification of the key structural and functional components of adipose tissue quality-including necrosis, senescence, inflammation, self-renewal, metabolic flexibility-and adipose tissue-secreted proteins that influence mobility via direct effects on skeletal muscle are necessary to prevent morbidity/mortality in the aging population.
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5.
Physiology of energy homeostasis: Models, actors, challenges and the glucoadipostatic loop.
Chapelot, D, Charlot, K
Metabolism: clinical and experimental. 2019;:11-25
Abstract
The aim of this review is to discuss the physiology of energy homeostasis (EH), which is a debated concept. Thus, we will see that the set-point theory is highly challenged and that other models integrating an anticipative component, such as energy allostasis, seem more relevant to experimental reports and life preservation. Moreover, the current obesity epidemic suggests that EH is poorly efficient in the modern human dietary environment. Non-homeostatic phenomena linked to hedonism and reward seem to profoundly impair EH. In this review, the apparent failed homeostatic responses to energy challenges such as exercise, cafeteria diet, overfeeding and diet-induced weight loss, as well as their putative determinants, are analyzed to highlight the mechanisms of EH. Then, the hormonal, neuronal, and metabolic factors of energy intake or energy expenditure are briefly presented. Last, this review focuses on the contributions of two of the most pivotal and often overlooked determinants of EH: the availability of endogenous energy and the pattern of energy intake. A glucoadipostatic loop model is finally proposed to link energy stored in adipose tissue to EH through changes in eating behavior via leptin and sympathetic nervous system activity.
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6.
The burden of metabolic syndrome on osteoarthritic joints.
Dickson, BM, Roelofs, AJ, Rochford, JJ, Wilson, HM, De Bari, C
Arthritis research & therapy. 2019;(1):289
Abstract
BACKGROUND The prevalence of osteoarthritis (OA) increases with obesity, with up to two thirds of the elderly obese population affected by OA of the knee. The metabolic syndrome (MetS), frequently associated with central obesity and characterised by elevated waist circumference, raised fasting plasma glucose concentration, raised triglycerides, reduced high-density lipoproteins, and/or hypertension, is implicated in the pathogenesis of OA. This narrative review discusses the mechanisms involved in the influence of MetS on OA, with a focus on the effects on macrophages and chondrocytes. MAIN TEXT A skewing of macrophages towards a pro-inflammatory M1 phenotype within synovial and adipose tissues is thought to play a role in OA pathogenesis. The metabolic perturbations typical of MetS are important drivers of pro-inflammatory macrophage polarisation and activity. This is mediated via alterations in the levels and activities of the cellular nutrient sensors 5' adenosine monophosphate-activated protein kinase (AMPK) and mammalian target of rapamycin complex 1 (mTORC1), intracellular accumulation of metabolic intermediates such as succinate and citrate, and increases in free fatty acids (FFAs) and hyperglycaemia-induced advanced glycation end-products (AGEs) that bind to receptors on the macrophage surface. Altered levels of adipokines, including leptin and adiponectin, further influence macrophage polarisation. The metabolic alterations in MetS also affect the cartilage through direct effects on chondrocytes by stimulating the production of pro-inflammatory and catabolic factors and possibly by suppressing autophagy and promoting cellular senescence. CONCLUSIONS The influence of MetS on OA pathogenesis involves a wide range of metabolic alterations that directly affect macrophages and chondrocytes. The relative burden of intra-articular versus systemic adipose tissue in the MetS-associated OA remains to be clarified. Understanding how altered metabolism interacts with joints affected by OA is crucial for the development of further strategies for treating this debilitating condition, such as supplementing existing therapies with metformin and utilising ω-3 fatty acid derivatives to restore imbalances in ω-3 and ω-6 fatty acids.
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7.
The complement system is dysfunctional in metabolic disease: Evidences in plasma and adipose tissue from obese and insulin resistant subjects.
Moreno-Navarrete, JM, Fernández-Real, JM
Seminars in cell & developmental biology. 2019;:164-172
Abstract
The relationship among chronic low-grade inflammation, insulin resistance and other obesity-associated metabolic disturbances is increasingly recognized. The possible mechanisms that trigger these immunologic alterations remain to be fully understood. The complement system is a crucial element of immune defense system, being important in the activation of innate and adaptative immune response, promoting the clearance of apoptotic and damaged endogenous cells and participating in processes of tissue development, degeneration, and regeneration. Circulating components of the complement system appear to be dysregulated in obesity-associated metabolic disturbances. The activation of the complement system is also evident in adipose tissue from obese subjects, in association with subclinical inflammation and alterations in glucose metabolism. The possible contribution of some components of the complement system in the development of insulin resistance and obesity-associated metabolic disturbances, and the possible role of complement system in adipose tissue physiology is reviewed here. The modulation of the complement system could constitute a potential target in the pathophysiology and therapy of obesity and associated metabolic disease.
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8.
Epicardial adipose tissue feeding and overfeeding the heart.
Iacobellis, G, Barbaro, G
Nutrition (Burbank, Los Angeles County, Calif.). 2019;:1-6
Abstract
Epicardial adipose tissue is a particular visceral fat depot with unique anatomic, biomolecular, and genetic features. Epicardial fat displays both physiological and pathological properties. Epicardial fat expresses genes and secretes cytokines actively involved in the thermogenesis and regulation of lipid and glucose metabolism of the adjacent myocardium. A disequilibrium between epicardial fat feeding and overfeeding the myocardium with free fatty acids leads to intramyocardial fat infiltration causing organ damage and clinical consequences. The upregulation of epicardial fat proinflammatory and lipogenic genes contributes to the fat build up in the proximal coronary arteries. Epicardial fat is a measurable and modifiable risk factor that can serve as a novel and additional tool for cardiovascular risk stratification. Pharmacologically targeting epicardial fat with drugs such as glucagon peptide-like 1 analogs or sodium glucose transport 2 inhibitors reduces the epicardial fat burden and induces beneficial cardiometabolic effects. Assessment and manipulation of epicardial fat transcriptome might open new avenues in the prevention of cardiometabolic diseases.
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9.
The Mesenteric Fat and Intestinal Muscle Interface: Creeping Fat Influencing Stricture Formation in Crohn's Disease.
Mao, R, Kurada, S, Gordon, IO, Baker, ME, Gandhi, N, McDonald, C, Coffey, JC, Rieder, F
Inflammatory bowel diseases. 2019;(3):421-426
Abstract
Adipose tissue is present in close proximity to various organs in the human body. One prominent example is fat contained in the mesentery that is contiguous with all abdominal digestive organs including the intestine. Despite the fact that mesenteric fat-wrapping around the inflamed gut (so called "creeping fat") was described as a characteristic feature of Crohn's disease (CD) in the early 1930s, the functional implications of creeping fat have received only recent attention. As a potent producer of fatty acids, cytokines, growth factors, and adipokines, creeping fat plays an important role in regulation of immunity and inflammation. Increasing evidence points to a link between creeping fat and intestinal inflammation in CD, where histopathologic evaluation shows a significant association between creeping fat and connective tissue changes in the bowel wall, such as muscular hypertrophy, fibrosis, and stricture formation. In addition, emerging mechanistic data indicate a link between creeping fat, muscularis propria hyperplasia, and stricturing disease. Information on fat-mesenchymal interactions in other organs could provide clues to fill the fundamental knowledge gap on the role of distinct components of creeping fat in intestinal fibrosis and stricture formation. Future studies will provide important new information that in turn could lead to novel therapeutic agents aimed at prevention or treatment of CD-associated fibrosis and stricture formation.
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10.
[Adipose tissue: immune function and alterations caused by obesity].
Vega-Robledo, GB, Rico-Rosillo, MG
Revista alergia Mexico (Tecamachalco, Puebla, Mexico : 1993). 2019;(3):340-353
Abstract
The adipose tissue, which is currently viewed as an organ with neuroimmunoendocrine functions, participates in the homeostasis of the human organism. It has great plasticity and functional variability based on the intake of nutrients or to the increase or decrease of its tissue volume, which modifies both the function and the number of the cells that form it or reach it. The elements that are released abnormally by these cells, among other cytokines and adipokines, cause both local and systemic inflammation, mainly when they come from the visceral adipose tissue, and they can affect diverse organs like the liver and the cardio-vascular system. It has been pointed out that obesity entails a greater risk for developing inflammatory, metabolic, autoimmune, or allergic diseases, as well as alterations in scarring, and cancer.