scholarly journals Modeling the Effect of High Calorie Diet on the Interplay between Adipose Tissue, Inflammation, and Diabetes

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
V. Prana ◽  
P. Tieri ◽  
M.C. Palumbo ◽  
E. Mancini ◽  
F. Castiglione

Background. Type 2 diabetes (T2D) is a chronic metabolic disease potentially leading to serious widespread tissue damage. Human organism develops T2D when the glucose-insulin control is broken for reasons that are not fully understood but have been demonstrated to be linked to the emergence of a chronic inflammation. Indeed such low-level chronic inflammation affects the pancreatic production of insulin and triggers the development of insulin resistance, eventually leading to an impaired control of the blood glucose concentration. On the contrary, it is well-known that obesity and inflammation are strongly correlated. Aim. In this study, we investigate in silico the effect of overfeeding on the adipose tissue and the consequent set up of an inflammatory state. We model the emergence of the inflammation as the result of adipose mass increase which, in turn, is a direct consequence of a prolonged excess of high calorie intake. Results. The model reproduces the fat accumulation due to excessive caloric intake observed in two clinical studies. Moreover, while showing consistent weight gains over long periods of time, it reveals a drift of the macrophage population toward the proinflammatory phenotype, thus confirming its association with fatness.

2019 ◽  
Vol 26 (19) ◽  
pp. 3593-3612
Author(s):  
Silvia Ezquerro ◽  
Amaia Rodríguez ◽  
Piero Portincasa ◽  
Gema Frühbeck

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.


PLoS ONE ◽  
2011 ◽  
Vol 6 (2) ◽  
pp. e17386 ◽  
Author(s):  
Bai Xue ◽  
Siddharth Sukumaran ◽  
Jing Nie ◽  
William J. Jusko ◽  
Debra C. DuBois ◽  
...  

2017 ◽  
Vol 23 (3) ◽  
pp. 131-146 ◽  
Author(s):  
Gisele Farias ◽  
Bárbara Dal Molin Netto ◽  
Solange Cravo Bettini ◽  
Ana Raimunda Dâmaso ◽  
Alexandre Coutinho Teixeira de Freitas

Introduction: Obesity, a serious public health problem, occurs mainly when food consumption exceeds energy expenditure. Therefore, energy balance depends on the regulation of the hunger–satiety mechanism, which involves interconnection of the central nervous system and peripheral signals from the adipose tissue, pancreas and gastrointestinal tract, generating responses in short-term food intake and long-term energy balance. Increased body fat alters the gut- and adipose-tissue-derived hormone signaling, which promotes modifications in appetite-regulating hormones, decreasing satiety and increasing hunger senses. With the failure of conventional weight loss interventions (dietary treatment, exercise, drugs and lifestyle modifications), bariatric surgeries are well-accepted tools for the treatment of severe obesity, with long-term and sustained weight loss. Bariatric surgeries may cause weight loss due to restriction/malabsorption of nutrients from the anatomical alteration of the gastrointestinal tract that decreases energy intake, but also by other physiological factors associated with better results of the surgical procedure. Objective: This review discusses the neuroendocrine regulation of energy balance, with description of the predominant hormones and peptides involved in the control of energy balance in obesity and all currently available bariatric surgeries. Conclusions: According to the findings of our review, bariatric surgeries promote effective and sustained weight loss not only by reducing calorie intake, but also by precipitating changes in appetite control, satiation and satiety, and physiological changes in gut-, neuro- and adipose-tissue-derived hormone signaling.


2016 ◽  
Vol 15 (3) ◽  
pp. 419-423
Author(s):  
Mariya Marushchak ◽  
Inna Krynytska ◽  
Lyudmyla Mazur ◽  
Svitlana Yastremska ◽  
Nina Begosh

Objective: According to WHO, about 30 % of people in the world are overweight that allows to characterize this disease as a new non-infection “epidemic” of the XXI century. More than 500 million people in the world are overweight and 250 million are obese. There is a clear tendency to increasing of alimentary obesity among people with different age, sex and nationality. The aim of the study is to investigate the thiol-disulfide homeostasis in liver tissue, adipose tissue and erythrocytes in the pathogenesis of experimental alimentary obesity.Materials and methods: 60 males, non-liner, white rats around 3 months of age with alimentary obesity were examined during the study. Experimental obesity was modeled by administering of sodium glutamate to the feed mixture in a ratio of 0.6:100.0 and adding high-calorie diet. The glutathione redox-system activity in erythrocytes, liver and adipose tissue were analyzed by the level of reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase (GR) and glutathione peroxidase (GP) activity.Results and Discussion: The data indicate a decrease in GSH level within 14 days of the experiment in all investigated tissues. The same trend was observed in animals on 28th day of the experiment: GSH index decreased in blood, adipose tissue and liver (P<0.05). The index of GSSG have increased on 28th day of the experiment in all investigated tissues vs control group (P<0.05). The ratio of the reduced and oxidized forms of glutathione contents was much lower vs control group in all the studied tissues within 28 days of the experiment. During additional investigation of the activity of thiol-disulfide system enzymes it was found that reducing the concentration of GSH in rats with alimentary obesity was due to the lack of thiol-disulfide system enzymes activity: GP and GR, which take part in the regeneration of GSH from GSSG.Conclusion: experimental alimentary obesity is characterized by a reduced redox state in blood, adipose and liver tissues, which is determinative in increasing the free radical reactions and accumulation of highly toxic lipoperoxides in the tissue substrates.Bangladesh Journal of Medical Science Vol.15(3) 2016 p.419-423


Author(s):  
O. V. Povarova ◽  
E. A. Gorodetskaya ◽  
E. I. Kalenikova ◽  
O. S. Medvedev

The article presents a modern view of obesity as a chronic inflammation of adipose tissue. Obesity is accompanied by metabolic changes in lipid, protein, carbohydrate, mineral metabolism and disorders in the hormonal function of adipose tissue as an endo- and paracrine organ. At the moment, there are searched the biochemical markers of metabolic disorders of obesity. The obesity-related factors (hyperglycemia, increased lipid levels, insulin resistance, chronic inflammation, hyperleptinemia, endothelial dysfunction, impaired respiratory function of mitochondria, minerals and microelements deficiency) form and increase oxidative stress making it an integral component of the pathogenesis of obesity and possible complications. Given the important role of Q10 coenzyme in antioxidant tissue protection, the authors discuss the relationship of obesity and metabolic disorders to the endogenous levels of Q10 coenzyme and its possible use for pharmacological correction.


Author(s):  
Leandro M Velez ◽  
Marcus Seldin ◽  
Alicia B Motta

Abstract Polycystic Ovary Syndrome (PCOS) is one of the most frequent endocrinopathies, affecting 5–10% of women of reproductive age, and is characterized by the presence of ovarian cysts, oligo, or anovulation, and clinical or biochemical hyperandrogenism [1]. Metabolic abnormalities such as hyperinsulinemia, insulin resistance, cardiovascular complications, dyslipidemia, and obesity are frequently present in PCOS women [1]. Several key pathogenic pathways overlap between these metabolic abnormalities, notably chronic inflammation. The observation that this mechanism was shared led to the hypothesis that a chronic inflammatory state could contribute to the pathogenesis of PCOS [2]. Moreover, while physiological inflammation is an essential feature of reproductive events such as ovulation, menstruation, implantation, and labour at term [3], the establishment of chronic inflammation may be a pivotal feature of the observed reproductive dysfunctions in PCOS women [2]. Taken together, the present work aims to review the available evidence about inflammatory mediators and related mechanisms in women with PCOS, with an emphasis on reproductive function.


Author(s):  
Evan M. Forman ◽  
Meghan L. Butryn

This chapter (Session 2) discusses the importance of self-monitoring to gain awareness of calorie intake and to recognize patterns in eating behavior. Clients are provided with information on how to self-monitor food intake, including recording type of food, serving size, method of preparation, and time of eating. Strategies for beginning to reduce calories are discussed, such as limiting high-calorie foods in the environment, eating regular meals, and planning meals in advance. The idea of achieving a negative energy balance is introduced, meaning that in order to lose weight, clients must expend a greater amount of energy than they consume in the form of calories.


Author(s):  
Elena Neumann ◽  
Klaus Frommer ◽  
Ulf Müller-Ladner

Adipokines, also called adipocytokines, are highly bioactive substances mainly expressed by adipose tissue. In addition to adipocytes, different cell types resident in various tissues produce adipokines under pathophysiological conditions. Adipokines include a growing number of pluripotent molecules such as adiponectin, resistin, leptin, and visfatin. Since distinct effects of adipokines on inflammation have been described, their influence on the (innate) immune system has been investigated in rheumatology, gastroenterology, and endocrinology. This review gives an overview on the current knowledge about the influence which adipokines have on the immune system and chronic inflammation in rheumatic diseases.


Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1037
Author(s):  
Alessandro Allegra ◽  
Giovanni Pioggia ◽  
Alessandro Tonacci ◽  
Marco Casciaro ◽  
Caterina Musolino ◽  
...  

Philadelphia-negative chronic myeloproliferative neoplasms (MPNs) have recently been revealed to be related to chronic inflammation, oxidative stress, and the accumulation of reactive oxygen species. It has been proposed that MPNs represent a human inflammation model for tumor advancement, in which long-lasting inflammation serves as the driving element from early tumor stage (over polycythemia vera) to the later myelofibrotic cancer stage. It has been theorized that the starting event for acquired stem cell alteration may occur after a chronic inflammation stimulus with consequent myelopoietic drive, producing a genetic stem cell insult. When this occurs, the clone itself constantly produces inflammatory components in the bone marrow; these elements further cause clonal expansion. In BCR–ABL1-negative MPNs, the driver mutations include JAK 2, MPL, and CALR. Transcriptomic studies of hematopoietic stem cells from subjects with driver mutations have demonstrated the upregulation of inflammation-related genes capable of provoking the development of an inflammatory state. The possibility of acting on the inflammatory state as a therapeutic approach in MPNs appears promising, in which an intervention operating on the pathways that control the synthesis of cytokines and oxidative stress could be effective in reducing the possibility of leukemic progression and onset of complications.


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