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Anorexia nervosa (AN) is characterised by the restriction of energy intake in relation to energy needs and a significantly lowered body weight than normally expected, coupled with an intense fear of gaining weight. Treatment of AN is currently based on psychological and refeeding approaches, but their efficacy remains limited since 40% of patients after 10 years of medical care still present symptoms of AN. The intestine hosts a large community of microorganisms, called the "microbiota", which live in symbiosis with the human host. The gut microbiota of a healthy human is dominated by bacteria from two phyla: Firmicutes and, majorly, Bacteroidetes. However, the proportion in their representation differs on an individual basis and depends on many external factors including medical treatment, geographical location and hereditary, immunological and lifestyle factors. Drastic changes in dietary intake may profoundly impact the composition of the gut microbiota, and the resulting dysbiosis may play a part in the onset and/or maintenance of comorbidities associated with AN, such as gastrointestinal disorders, anxiety and depression, as well as appetite dysregulation. Furthermore, studies have reported the presence of atypical intestinal microbial composition in patients with AN compared with healthy normal-weight controls. This review addresses the current knowledge about the role of the gut microbiota in the pathogenesis and treatment of AN. The review also focuses on the bidirectional interaction between the gastrointestinal tract and the central nervous system (microbiota–gut–brain axis), considering the potential use of the gut microbiota manipulation in the prevention and treatment of AN. [ABSTRACT FROM AUTHOR]

To evaluate the short- (within 90 min) and long-term (after 21 days of treatment) effects of an artificial tear containing carbomer, hyaluronic acid, glycerol, and medium-chain triglycerides in patients with mild-to-moderate dry eye symptoms. Subjects received the tested artificial tears in the right eye and control artificial tears in the left eye and were assessed 10, 30, 60, and 90 min after instillation in the short-term study phase. They received the study product in both eyes in the long-term phase. Non-invasive break-up time (NIBUT), tear lipid layer pattern, tear evaporation, and tear film objective optical dynamics (TFOOD) were measured in controlled environmental conditions. In total, 32 patients (10 males, mean age 42 ± 11 years) were enrolled. During the short-term phase, NIBUT increased significantly in the right eyes at all time points compared with baseline (all p < 0.05). Conversely, in the left eyes, NIBUT increased significantly at 10 and 30 min (p < 0.05). The tear evaporation values increased at 10 min and decreased at 30 and 60 min (p < 0.05) in the right eyes, while they increased only at 10 min (p < 0.05) in the left eyes. Compared with baseline, the TFOOD was significantly more stable at all time points in the right eyes (p < 0.05), while it was more stable at 10 and 30 min in the left eyes (p < 0.05). In the long-term phase, treated eyes showed a significant increase in NIBUT values, a significant reduction of tear evaporation, a significant improvement of tear lipid layer pattern, and a more stable TFOOD compared with baseline (all p < 0.05). Symptoms, measured with the Ocular Surface Disease Index questionnaire, were also significantly reduced compared with baseline (p < 0.05). The tested product increased tear film stability and reduced tear evaporation, normalizing lipid layer pattern and reducing symptoms in the short- and long-term observation. [ABSTRACT FROM AUTHOR]

Lysosomal storage disorders (LSDs) are a group of clinically heterogeneous disorders affecting the function of lysosomes and are characterized by an accumulation of undigested substrates within several cell types. In recent years there have been substantial advances in supportive care and drug treatment for some LSDs, leading to improved patient survival, as seen in Gaucher, Pompe and Fabry disease and some Mucopolysaccharidoses; however, many symptoms still persist. Thus it is now even more important to improve patients' quality of life and reduce symptoms and comorbidities. One potential way of achieving this goal is through adjunct nutritional therapy, which is challenging as patients may be overweight with associated consequences, or malnourished, or underweight. Furthermore, drugs used to treat LSDs can modify the metabolic status and needs of patients. There are currently not enough data to make specific dietary recommendations for individual LSDs; however, suggestions can be made for managing clinical manifestations of the diseases, as well as treatment-associated adverse events. The metabolic and nutritional status of adult patients must be regularly assessed and individualized dietary plans may be created to cater to a patient's specific needs. Damage to the autophagic process is a common feature in LSDs that is potentially sensitive to dietary manipulation and needs to be assessed in clinical studies. [ABSTRACT FROM AUTHOR]

Background: Fabry disease is characterized by deficient expression/activity of α-GalA with consequent lysosomal accumulation in various organs of its substrate Gb3. Despite enzyme replacement therapy, Fabry disease progresses with serious myocardial, cerebral and renal manifestations. Gb3 accumulation may induce oxidative stress (OxSt), production of inflammatory cytokines and reduction of nitric oxide, which may impact on Fabry disease’s clinical manifestations. Methods: OxSt status was characterized in 10 patients compared with 10 healthy subjects via protein expression of p22phox, subunit of NADH/NADPH oxidase, (Western blot), Heme oxygenase (HO)-1 levels (ELISA), antioxidant/anti-inflammatory, lipid peroxidation as malondialdehyde (MDA) production (colorimetric assay), phosphorylation state of Extracellular Signal Regulated Kinase (ERK)1/2 and Myosin Phosphatase Target Protein (MYPT)-1 (Western blot), marker of Rho kinase activation, both involved in OxSt signaling. Cardiac left ventricular (LV) mass was also evaluated (M-mode echocardiography). Results: LV mass was higher in Fabry’s males (123.72±2.03SEM g/m2) and females (132.09±6.72g/m2). p22phox expression was also higher in patients (1.04±0.09 d.u. vs 0.54±0.05 d.u. p<0.01) as well as MDA levels (54.51±3.97 vs 30.05±7.11 nmol/mL p = 0.01) while HO-1 was reduced (8.84±0.79 vs 14.03±1.23 ng/mL, p<0.02). MYPT-1’s phosphorylation was increased in patients (0.52±0.11 d.u. vs 0.03±0.08 d.u., p<0.01) while phosphorylation of ERK1/2 was reduced (0.91±0.08 d.u. vs 1.53±0.17 d.u., p = 0.004). Conclusions: This study documents OxSt activation and the altered reaction to it in Fabry patients. Cardiac remodeling, Rho kinase signaling activation and reduction of protective HO-1 might suggest that, in addition to enzyme replacement therapy, OxSt inhibition by either pharmacological or nutritional measures, is likely to prove useful for the prevention/treatment of Fabry patients’ cardiovascular-renal remodeling. [ABSTRACT FROM AUTHOR]

Body fat accumulation, distribution, and metabolic activity are factors in the pathophysiology of obesity and type 2 diabetes (T2D). We investigated adipose blood flow, fatty acid uptake (FAU), and subcutaneous and visceral fat cellularity in obese patients with or without T2D. A total of 23 morbidly obese (mean body mass index = 42 kg/m²) patients were studied before and 6 mo after bariatric surgery; 15 nonobese subjects served as controls. Positron emission tomography was used to measure tissue FAU (with 18F-FTHA) and blood flow (with H2 15O); MRI was used for fat distribution and fat biopsy for adipocyte size. Obese subjects had subcutaneous hyperplasia and hypertrophy and lower blood flow; when expressed per cell, flow was similar to controls. FAU into subcutaneous and visceral depots was increased in the obese; per unit tissue mass, however, FAU was similar to controls but reduced in skeletal muscle. Fatty acid fractional extraction in subcutaneous fat and muscle was only increased in obese patients with T2D. We conclude that surgery reduces subcutaneous fat hyperplasia and hypertrophy; subcutaneous blood flow and FAU decrease in absolute terms and per cell while fractional FAU remains unchanged in T2D. In the obese, subcutaneous blood flow is a determinant of FAU and is coupled with cellularity; efficiency of FAU is enhanced in subcutaneous fat and muscle in T2D. [ABSTRACT FROM AUTHOR]

Objective: We investigated fat distribution and tissue-specific insulin-stimulated glucose uptake (GU) in seven fat compartments (visceral and subcutaneous) and skeletal muscle in morbidly obese patients with (T2D) and without (ND) type 2 diabetes before and 6 months after bariatric surgery.Research Design and Methods: A total of 23 obese patients (BMI 43.0 ± 3.6 kg/m(2); 9 T2D and 14 ND) were recruited from a larger, randomized multicenter SLEEVEPASS study. MRI (for fat distribution) and [(18)F]-fluorodeoxyglucose PET (for GU) studies were performed for the obese patients before and 6 months postsurgery; 10 lean subjects served as control subjects and were studied once.Results: At baseline, visceral fat GU was 30 ± 7% of muscle GU in control subjects and 57 ± 5% in obese patients. Visceral and deep subcutaneous fat were more abundant (despite same total fat mass) and less insulin sensitive in T2D than ND; in both, GU was impaired compared with control subjects. Postsurgery, visceral fat mass decreased (∼40%) more than subcutaneous fat (7%). Tissue-specific GU was improved, but not normalized, at all sites in T2D and ND alike. The contribution of visceral fat to whole-body GU was greater in T2D than ND but decreased similarly with surgery. Subcutaneous fat made a fourfold greater contribution to whole-body GU in obese versus lean subjects (15% vs. 4%) both before and after surgery.Conclusions: Bariatric surgery leads to sustained weight loss and improves tissue-specific glucose metabolism in morbidly obese patients. We conclude that 1) enhanced visceral fat accumulation is a feature of T2D, 2) severe obesity compromises muscle insulin sensitivity more than fat insulin sensitivity, and 3) fat mass expansion is a sink for plasma glucose. [ABSTRACT FROM AUTHOR]

Introduction: The prevalence of overweight, obesity, and their related complications is increasing worldwide. We aimed to summarise and critically evaluate the effects of different popular diets on anthropometric parameters and metabolic risk factors. Material and methods: An umbrella review of meta-analyses of randomized controlled trials was conducted according to the Joanna Briggs Institute Umbrella Review Methodology. The review protocol has been registered on PROSPERO (ID: CRD42019126103). Medline, Embase, Scopus, Cochrane Database of Systematic Reviews, and Web of Science were searched from inception to April 2019 to identify meta-analyses of randomized controlled trials that examined the effects of different diets on anthropometric parameters and metabolic risk factors. For each association, we estimated the summary effect size by random-effects and fixed-effects models, the 95% confidence interval, and the 95% prediction interval. We also assessed the between-study heterogeneity and evidence for small-study effects. We further applied standardized methodological criteria to evaluate the epidemiological credibility of the statistically significant associations. Results: Overall, 80 articles reporting 495 unique meta-analyses were examined, covering a wide range of popular diets: low-carbohydrate (n = 21 articles), high-protein (n = 8), low-fat (n = 9), palaeolithic (n = 2), low glycaemic index/load (n = 12), intermittent energy restriction (n = 6), Mediterranean (n = 11), Nordic (n = 2), vegetarian (n = 9), Dietary Approaches to Stop Hypertension or DASH (n = 6), and portfolio dietary pattern (n = 1). The methodological quality of most articles (n = 65; 81%), evaluated using the AMSTAR-2 questionnaire, was low or critically low. The strength of evidence was generally weak. The most consistent evidence was reported for Mediterranean diet, with suggestive evidence of an improvement in weight, body mass index (BMI), total cholesterol, glucose and blood pressure. Suggestive evidence of an improvement in weight and blood pressure was also reported for DASH diet. Low-carbohydrate, high-protein, low-fat and low-glycaemic index/load diets showed suggestive and/or weak evidence of a reduction in weight and BMI, but contrasting evidence for lipid, glycaemic and blood pressure parameters, suggesting potential risks of unfavourable effects. Finally, evidence for palaeolithic, intermittent energy restriction, Nordic, vegetarian and portfolio dietary patterns was graded as weak or not statistically significant. Discussion: Most meta-analyses showed low methodological quality and the strength of evidence, assessed using evidence classification criteria, was generally weak. Among all the diets evaluated, Mediterranean diet had the strongest and most consistent evidence of a positive effect on both anthropometric parameters and metabolic risk factors. [ABSTRACT FROM AUTHOR]

Sarcopenia is a progressive clinical syndrome characterized by general loss of skeletal muscle mass and impaired muscle function. Due to the general progressive aging of population, sarcopenia has gradually grown into a global health problem, with great negative impact on the quality of life of the affected patients as well as an adverse societal impact. In this review, we discuss the pathophysiology, diagnosis, and determination of severity of sarcopenia. Special attention is given to the rehabilitative treatment against sarcopenia, pointing out that a thorough evaluation and intervention of nutritional deficits and exercise capacity as well as treatment with medical agents are needed in order to personalize the treatment according to the patient's needs. By targeting goals to improve musculoskeletal and functional disorders associated with chronic conditions, clinicians could apply a therapeutic plan focusing on how to prevent/delay the development of sarcopenia and improve the quality of the patients' lives.

Cardiovascular diseases (CVD) are the leading cause of death worldwide. Evidence from observational and randomized controlled studies showing the potential benefits of green tea on lowering CVD risk has been emerging rapidly during the past few decades. These benefits include reduced risk for major cardiovascular events, lowering of blood pressure, decreased LDL cholesterol levels and weight loss. At the same time, the understanding of the physiological mechanisms behind these alterations is advancing. Consumption of green tea originated from China thousands of years ago, but since then, it expanded all over the world. Recent advances in understanding the role of tea polyphenols, mainly catechins, as mediators of tea's health benefits, have caused the emergence of various types of green tea extracts (GTE) on the market. While taking green tea is generally considered safe, there are concerns about the safety of using tea extracts. The present article reviews the current evidence of green tea consumption leading to reduced CVD risk, its potential biological mechanisms and the safety of using GTE., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Obesity, a chronic low-grade inflammation disorder characterized by an expansion in adipose tissue mass, is rapidly expanding worldwide leading to an increase in the incidence of comorbidities such as insulin resistance, type 2 diabetes and cardiovascular diseases. This has led to a renewed interest in the adipose tissue function, historically considered as a passive fat storage. It is now well established that adipose tissue is an organ with an active role in production and release of a variety of molecules called adipocytokines. Dysregulated production of adipocytokines seems to be responsible for the pathogenesis of insulin resistance and type 2 diabetes; however, the mechanisms are still unclear. Hypoxia, that occurs when adipocytes expand in obesity, has been proposed as a possible cause of adipose tissue inflammation. On the other hand, recent studies have shown that adipose tissue oxygen tension was actually higher (hyperoxia) than normal and associated with insulin resistance in obesity, despite a reduction in blood flow. This might be explained by the role of mitochondrial oxygen consumption. Hence, further studies are needed to understand the role of adipose tissue oxygenation and perfusion in obesity to assess pathophysiology and novel opportunities for treating the diseases.

Cardiovascular risk factors, irregardless of their assessment modalities, are based on cardiovascular health. Lifestyle influences metabolic profiles and these changes affect cardiovascular risk factors. Cardiovascular risk factors can be classified into three basic categories: 1. Predisposing risk factors (e.g., age, gender, medical history, and genetic factors); 2. Clinical and metabolic factors (e.g., hypertension, changes in lipid metabolism, diabetes mellitus, obesity, metabolic syndrome, homocysteine, serum uric acid concetntrations, and L-arginine dimethylated derivatives); 3. Modifying behavioral factors (e.g., cigarette smoking, high caloric diet, alcohol intake, sedentary life). Some of these factors are metabolic components of body metabolism because they act by metabolic reactions while others characterized by structural alterations of the cardiovascular system, at least initially, exert their harmful effects by metabolic substrates. Metabolic responses such as biochemical substances, drugs or others, that act initially as cardiovascular risk factors, identify that an early treatment of the altered parameters observed should be a useful approach to reduce the rate of heart attacks with a significant improvement in the outcome of cardiovascular disease.

Both conduit and resistance arterial vessels may show vascular morphological and functional alterations due to cigarette smoking. Pathological lesions involve the arterial wall or intravascular lumen with, primarily, narrowing and thrombo-embolic events as an effect of endothelial and blood cell changes related to smoking. Functional disorders are the result of a wide spectrum of biochemical, physiological and metabolic factors. While conduit vessel alterations have been widely investigated, little is known about the changes induced by smoking on the microcirculation. It would seem that the endothelium, platelet aggregation and adhesiveness, nervous system and metabolic changes play a role in damaging resistance arteries and, then, the microcirculation. The result of these effects changes the blood flow and perfusion particularly to the heart, brain and kidney. Alterations of the microcirculation can cause severe and widespread damage because, in addition to the complications of the atherosclerotic lesion which characterizes large arteries, there is a failure of body organs linked to the degree of microvascular damage. Moreover, it seems that 2 major compounds of cigarette smoke are capable of determining vascular damage; initially, nicotine acts preferably on large arteries and carbon monoxide on small arteries, although both compounds damage the vascular system.

Significant technical advances in small animal molecular imaging techniques and in imaging probes with high specificity for various molecular targets have been produced in the last ten years. Notwithstanding, the clinical applicability of molecular imaging proceeds slowly. In animal experiments, multimodality molecular imaging techniques based on hybrid scanners are increasing, providing more insight into path physiologic phenomena associated with cardiovascular disease. In parallel, we assisted in the development of a new generation of multi-imaging probes, such as PET/MRI probes, particularly effective in hybrid scanners. More recently, in order to gain in inherently low sensitivity of MRI, hyperpolarized magnetic resonance spectroscopy using hyperpolarized (13)C was proposed. Preliminary results obtained in experimental animal studies seem to confirm the potentialities of hyperpolarized (13)C magnetic resonance to monitor myocardial energetics. In this review the preclinical cardiovascular applications and the potential for clinical translation are discussed.

Ultrasound assessment of vascular biomarkers has been implemented for screening, prevention and improvement of cardiovascular risk stratification beyond classical risk factors including smoking, diabetes, hypercholesterolemia and hypertension. Thus, the presence of vascular damage at the sub-clinical, asymptomatic stages can identify a "vulnerable" patient, and aid in implementing cardiovascular prevention strategies. Increased intima-media thickness of the common carotid artery is a well-known marker of early atherosclerosis, which significantly correlates with the development of coronary or cerebro-vascular disease. More recently, guidelines for cardiovascular prevention in hypertension also introduced other vascular parameters evaluating both mechanical and functional arterial properties of peripheral arteries. Increased arterial stiffness, which can be detected by ultrasound at the common carotid, has been shown to predict future cardiovascular events and it is already considered a subclinical target organ of hypertensive patients. Even earlier vascular abnormalities such as endothelial dysfunction in the peripheral arteries, detected as reduced flow-mediated dilation of the brachial artery by ultrasound, have also been mentioned for their possible clinical use in the future. This manuscript reviews clinical evidence supporting the use of these different vascular markers for cardiovascular risk stratification, focusing on the need for an accurate, robust and reliable methodology for the assessment of vascular markers, which could improve their predictive value and increase their use in routine clinical practice.

Changes in clinical, biochemical and pathological variables characterize cardiovascular damage from smoking and hypertension when it acts independently. However, combined action of these major risk factors increases the rate of cardiovascular events. Ischaemic heart disease with stable effort angina, myocardial infarction and post-infarction arrhythmias may affect cardiovascular system because of smoking exposure. Among cerebrovascular disease, there is evidence that stroke would be related primarily to active smoking. Isolated hypertension plays significantly major action to cause cerebrovascular disease including stroke, recurrent stoke and transient ischaemic attack. Among cardiac events, heart failure is, often, the end-point of hypertensive disease, even if manifestations of ischaemic heart disease similar to those caused by smoking may be increased in rate. Combined action of smoking and hypertension usually increases the rate of cardiovascular complications and leads to a progression of atherosclerosis with narrowing and plaque primarily at the the level of coronary, carotid and cerebrovascular arteries. A pattern specific of both active and passive smoking exposure, but not hypertension, is the thromboangiitis obliterans that dramatically worsens in continuing smokers while it can be improved by stopping smoking.

This article reviews the current imaging techniques and the methodologies used to derive quantitative markers of hypertension in the cardiovascular system. Firstly, simple but effective methods to assess regional and global function of large arteries are discussed. After, the role of echocardiography and high-resolution magnetic resonance imaging to assess geometric and mechanical indices of hypertension related cardiac diseases are summarized. In particular, quantitative indices of deformation and strain are derived from quantitative analysis of doppler tissue and tagged magnetic resonance images. Finally, the importance of high field magnetic resonance imaging to assess myocardial microcirculation is described.

Epidemiological surveys demonstrate undoubtedly that cardiovascular disorders caused or associated with hypertension are at a high risk of non-fatal or fatal events and occurring with a great rate. Ischaemic heart disease with effort angina and myocardial infarction, often unrecognized myocardial infarction, stroke and transient ischaemic attack may be observed more frequently than other cardiovascular disorders in hypertensive patients. Large-scale trials do not support the hypothesis that effective benefits are reached by current non-pharmacological or pharmacological prevention which need enormous costs to public health. Lowering blood pressure is the main target to reach in an attempt to reduce cardiovascular complications in hypertensive patients. Therefore, the costs-benefit ratio, which estimates public health costs, needs yet marked improvement since the public health expenses are heaviest with results that do not support the economic effort. Statistically, quantitative measures to modify the current regimen need to better evaluate both public health costs and reached benefits.

The definition of smoking as the inhalation of the smoke of burned tobacco that may occur occasionally or habitually as a consequence of a physical addiction to some chemicals, primarily nicotine, cannot be fully accepted today since several clinical, biological, metabolic, epidemiologic, statistic and socio-economic factors which play a basic role in determining individual damage due to smoking are missing in this assessment. The analysis of findings shows undoubtedly that several constituents of cigarette smoking play a strong role in the development and progression of cardiovascular damage, primarily atherosclerotic lesions. Nicotine and its metabolites, carbon monoxide and thiocyanate seem to be the most specific markers of damage that, in the time, becomes irreversible. Cigarette smoking is addictive because of nicotine and nicotine withdrawal causes many side effects of quitting smoking as well as nicotine itself usually increases cardiovascular risk. Therefore, what is smoking? Smoking must be defined as a chemical toxicosis which is able to cause detrimental effects either of acute or chronic type on different structures of the body being some of these like cardiovascular system, respiratory system and epithelial glands target organs. Smoking also causes physical addiction, primarily due to nicotine, that adversely influences smoking cessation. From these observations there is evidence that a large number of socio-economic and epidemiologic implications arise in smokers and that requires the necessity of specific structures which may help to face up the problem.

This article reviews the current techniques employed to assess endothelial dysfunction in different categories of smokers. Simple but effective methods to assess regional and local properties of large arteries for epidemiologic studies are firstly discussed. After, more complex but accurate image-based methods are described. In particular, the role of high resolution magnetic resonance to quantify, in a single examination, vascular function at different sites of peripheral and central arteries is summarized. Finally, the role of positron emission tomography and magnetic resonance flow mapping are described to assess myocardial microcirculation at rest and under external stressors.

Tobacco smoking remains the second largest preventable cause of mortality and morbidity worldwide. Exposure to tobacco smoke causes coronary disease, atherosclerosis and ischemic vessel disease. The degree of this risk is proportional to the amount of smoking and it varies from individual to individual because of between-individual differences in genetic background. While the chemical properties of tobacco smoke are relatively well characterized, the mechanisms by which smoking leads to disease and the genetic factors that determine susceptibility to these diseases are not well understood. The purpose of the present review is to describe the interaction between DNA variants in some important genes and cardiovascular diseases; and how the exposure to cigarette smoke significantly modifies the association between genetic variants and cardiovascular risk. A great number of gene-enzymes that usually protect against cardiovascular events may be adversely influenced by tobacco smoke and, through this way, exert less effective action.

In this review, we will give a critical update of published studies using ultrasound for targeted therapeutic use. We will briefly discuss the interaction mechanisms and their effects in non-invasive delivery of therapeutic agents. Moreover, the mechanisms by which ultrasonic contrast agents facilitate the delivery of drugs and genes into tissue will be discussed, together with recent applications and perspectives of targeted-microbubbles in cardiovascular medicine.