scholarly journals Drugs Involved in Dyslipidemia and Obesity Treatment: Focus on Adipose Tissue

2018 ◽  
Vol 2018 ◽  
pp. 1-21 ◽  
Author(s):  
Sofia Dias ◽  
Sílvia Paredes ◽  
Laura Ribeiro

Metabolic syndrome can be defined as a state of disturbed metabolic homeostasis characterized by visceral obesity, atherogenic dyslipidemia, arterial hypertension, and insulin resistance. The growing prevalence of metabolic syndrome will certainly contribute to the burden of cardiovascular disease. Obesity and dyslipidemia are main features of metabolic syndrome, and both can present with adipose tissue dysfunction, involved in the pathogenic mechanisms underlying this syndrome. We revised the effects, and underlying mechanisms, of the current approved drugs for dyslipidemia and obesity (fibrates, statins, niacin, resins, ezetimibe, and orlistat; sibutramine; and diethylpropion, phentermine/topiramate, bupropion and naltrexone, and liraglutide) on adipose tissue. Specifically, we explored how these drugs can modulate the complex pathways involved in metabolism, inflammation, atherogenesis, insulin sensitivity, and adipogenesis. The clinical outcomes of adipose tissue modulation by these drugs, as well as differences of major importance for clinical practice between drugs of the same class, were identified. Whether solutions to these issues will be found in further adjustments and combinations between drugs already in use or necessarily in new advances in pharmacology is not known. To better understand the effect of drugs used in dyslipidemia and obesity on adipose tissue not only is challenging for physicians but could also be the next step to tackle cardiovascular disease.

2016 ◽  
Vol 64 (4) ◽  
pp. 830-832 ◽  
Author(s):  
Neda Rasouli

Despite the well-established association of obesity with insulin resistance and inflammation, the underlying mechanisms and sequence of events leading to inflammation and insulin resistance remain unknown. Adipose tissue hypoxia has been proposed as one of the possible key events during the process of fat expansion that leads to adipose tissue dysfunction. The focus of this paper is reviewing the evidence on adipose tissue hypoxia in obesity and its relation to insulin resistance.


2020 ◽  
Vol 21 (14) ◽  
pp. 4860 ◽  
Author(s):  
Michele Mannelli ◽  
Tania Gamberi ◽  
Francesca Magherini ◽  
Tania Fiaschi

Cachexia is a devastating pathology induced by several kinds of diseases, including cancer. The hallmark of cancer cachexia is an extended weight loss mainly due to skeletal muscle wasting and fat storage depletion from adipose tissue. The latter exerts key functions for the health of the whole organism, also through the secretion of several adipokines. These hormones induce a plethora of effects in target tissues, ranging from metabolic to differentiating ones. Conversely, the decrease of the circulating level of several adipokines positively correlates with insulin resistance, metabolic syndrome, diabetes, and cardiovascular disease. A lot of findings suggest that cancer cachexia is associated with changed secretion of adipokines by adipose tissue. In agreement, cachectic patients show often altered circulating levels of adipokines. This review reported the findings of adipokines (leptin, adiponectin, resistin, apelin, and visfatin) in cancer cachexia, highlighting that to study in-depth the involvement of these hormones in this pathology could lead to the development of new therapeutic strategies.


2009 ◽  
Vol 118 (4) ◽  
pp. 231-240 ◽  
Author(s):  
Carmine Savoia ◽  
Massimo Volpe ◽  
Alessandro Alonzo ◽  
Chiara Rossi ◽  
Speranza Rubattu

Natriuretic peptides are endogenous antagonists of vasoconstrictor and salt- and water-retaining systems in the body's defence against blood pressure elevation and plasma volume expansion, through direct vasodilator, diuretic and natriuretic properties. In addition, natriuretic peptides may play a role in the modulation of the molecular mechanisms involved in metabolic regulation and cardiovascular remodelling. The metabolic syndrome is characterized by visceral obesity, hyperlipidaemia, vascular inflammation and hypertension, which are linked by peripheral insulin resistance. Increased visceral adiposity may contribute to the reduction in the circulating levels of natriuretic peptides. The dysregulation of neurohormonal systems, including the renin–angiotensin and the natriuretic peptide systems, may in turn contribute to the development of insulin resistance in dysmetabolic patients. In obese subjects with the metabolic syndrome, reduced levels of natriuretic peptides may be involved in the development of hypertension, vascular inflammation and cardio vascular remodelling, and this may predispose to the development of cardiovascular disease. The present review summarizes the regulation and function of the natriuretic peptide system in obese patients with the metabolic syndrome and the involvement of altered bioactive levels of natriuretic peptides in the pathophysiology of cardiovascular disease in patients with metabolic abnormalities.


2004 ◽  
Vol 29 (6) ◽  
pp. 808-829 ◽  
Author(s):  
Lindsay E. Robinson ◽  
Terry E. Graham

The metabolic syndrome comprises an array of cardiovascular disease (CVD) risk factors such as abdominal obesity, dyslipidemia, hypertension, and glucose intolerance. Insulin resistance and/or increased abdominal (visceral) obesity have been suggested as potential etiological factors. More recently, increasing evidence has associated insulin resistance and subclinical inflammation involving cytokines derived from adipose tissue, or adipocytokines. Despite the fact that precise mechanisms have yet to be established, there is a significant role for both diet and physical activity to improve the many factors associated with the metabolic syndrome, including modulation of various adipocytokines. Although both diet and physical activity have been studied for their ability to modify cytokines in more traditional inflammatory conditions, such as rheumatoid arthritis, they have been less studied in relation to inflammation as an underlying cause of the metabolic syndrome and/or CVD. A more thorough understanding of the clustering of metabolic abnormalities and their underlying etiology will help to define diet and physical activity guidelines for preventing and treating the metabolic syndrome, an important aspect of CVD prevention. This paper will address potential underlying causes of the metabolic syndrome, with a focus on the putative mechanistic role of adipocytokines, and will discuss the impact of diet and physical activity on the metabolic syndrome. Key words: insulin resistance syndrome, obesity, adipose tissue, skeletal muscle, cytokines, TNF-α, IL-6, PAI-1, inflammation, nutrition, exercise


2021 ◽  
Vol 18 (2) ◽  
pp. 142-149
Author(s):  
A. F. Verbovoy ◽  
N. I. Verbovaya ◽  
Yu. A. Dolgikh

Metabolic syndrome is a symptom complex that is based on visceral obesity and insulin resistance. Its prevalence is quite high, which is a big problem, since this condition increases the risk of developing cardiovascular diseases and mortality from them. Metabolic syndrome includes, in addition to abdominal obesity, arterial hypertension, disorders of carbohydrate, lipid and purine metabolism. Visceral adipose tissue plays a key role in the formation of insulin resistance and other components of the metabolic syndrome. This is due to the fact that abdominal fat, in contrast to subcutaneous fat, synthesizes pro-inflammatory cytokines, as well as adipokines — adipose tissue hormones that are involved in the formation of insulin resistance, affect carbohydrate and fat metabolism and the cardiovascular system. These include leptin, adiponectin, resistin, apelin and others. Some adipokines have an adverse effect on metabolism and increase cardiovascular risks, while others, on the contrary, have a positive effect. Taking into account their role in the development of the components of the metabolic syndrome, the possibilities of a therapeutic effect on the hormones of adipose tissue to improve metabolic processes and prevent complications associated with it are discussed.


Author(s):  
A. L. Zagayko ◽  
D. V. Lytkin ◽  
A. V. Maloshtan

Introduction. Nowadays, about 86 % among patients with metabolic syndrome have serious disorder of glucose tolerance and about 60 % of them suffer from visceral obesity. Moreover in many worldwide studies it was shown that these pathogenetic manifestations of the metabolic syndrome had a significant correlation with the imbalance of sex hormones.The aim of the study – to learn the effect of third-generation aromatase inhibitors on the parameters of insulin resistance and visceral obesity in hamsters with the experimental metabolic syndrome.Research Methods. The insulin level in the hamster`s blood serum was measured by the enzyme immunoassay method, and the glucose level by the electrochemical method. The mass coefficients of anatomical fragments of adipose tissue were calculated to estimate visceral obesity. The results were processed by using the Mann-Whitney U-test and the 4Pl method.Results and Discussion. All studied drugs, in varying degrees, influenced on the pathogenetic components of the experimental metabolic syndrome. Exemestane was demonstrated the greatest effectiveness in reducing parameter of the insulin resistance by, butletrozole – in decreasing of visceral obesity ratio.Сonclusion. Romatase inhibitors can become promising drugs for correcting the pathogenetic components of the metabolic syndrome, in particular insulin resistance and visceral obesity.


2014 ◽  
Vol 2014 ◽  
pp. 1-21 ◽  
Author(s):  
Jaspinder Kaur

Metabolic syndrome is defined by a constellation of interconnected physiological, biochemical, clinical, and metabolic factors that directly increases the risk of cardiovascular disease, type 2 diabetes mellitus, and all cause mortality. Insulin resistance, visceral adiposity, atherogenic dyslipidemia, endothelial dysfunction, genetic susceptibility, elevated blood pressure, hypercoagulable state, and chronic stress are the several factors which constitute the syndrome. Chronic inflammation is known to be associated with visceral obesity and insulin resistance which is characterized by production of abnormal adipocytokines such as tumor necrosis factorα, interleukin-1 (IL-1), IL-6, leptin, and adiponectin. The interaction between components of the clinical phenotype of the syndrome with its biological phenotype (insulin resistance, dyslipidemia, etc.) contributes to the development of a proinflammatory state and further a chronic, subclinical vascular inflammation which modulates and results in atherosclerotic processes. Lifestyle modification remains the initial intervention of choice for such population. Modern lifestyle modification therapy combines specific recommendations on diet and exercise with behavioural strategies. Pharmacological treatment should be considered for those whose risk factors are not adequately reduced with lifestyle changes. This review provides summary of literature related to the syndrome’s definition, epidemiology, underlying pathogenesis, and treatment approaches of each of the risk factors comprising metabolic syndrome.


2020 ◽  
Vol 1 (2) ◽  
pp. 77-85
Author(s):  
Arun K. Chopra

Metabolic syndrome is a clinical entity characterized by abdominal obesity, atherogenic dyslipidemia, impaired glucose tolerance, and hypertension (HT). Despite various attempts at definition, the syndrome has remained mired in controversy over its components and utility. Insulin resistance and its association with risk of cardiovascular disease are discussed at length in this article. This review also discusses the controversies in the definition of this syndrome, the unique role of insulin resistance in its development, and the causes and implications of this clustering of risk factors characteristic to it, along with suggestions for a more comprehensive approach to this common problem.


2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Andrew A. Bremer ◽  
Ishwarlal Jialal

The metabolic syndrome (MetS) confers an increased risk for both type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Moreover, studies on adipose tissue biology in nascent MetS uncomplicated by T2DM and/or CVD are scanty. Recently, we demonstrated that adipose tissue dysregulation and aberrant adipokine secretion contribute towards the syndrome’s low-grade chronic proinflammatory state and insulin resistance. Specifically, we have made the novel observation that subcutaneous adipose tissue (SAT) in subjects with nascent MetS has increased macrophage recruitment with cardinal crown-like structures. We have also shown that subjects with nascent MetS have increased the levels of SAT-secreted adipokines (IL-1, IL-6, IL-8, leptin, RBP-4, CRP, SAA, PAI-1, MCP-1, and chemerin) and plasma adipokines (IL-1, IL-6, leptin, RBP-4, CRP, SAA, and chemerin), as well as decreased levels of plasma adiponectin and both plasma and SAT omentin-1. The majority of these abnormalities persisted following correction for increased adiposity. Our data, as well as data from other investigators, thus, highlight the importance of subcutaneous adipose tissue dysfunction in subjects with MetS and its contribution to the proinflammatory state and insulin resistance. This adipokine profile may contribute to increased insulin resistance and low-grade inflammation, promoting the increased risk of T2DM and CVD.


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