Metabolic Diseases: a differential diagnosis of primary progressive multiple sclerosis

Objectives: The overall aim of our research project is to develop a Next Generation Sequencing strategy to identify metabolic disorders in 104 patients with a presumptive diagnosis of primary progressive MS.We would like to thank to MERCK, SA and NORTE2020 (NORTE-01-0246-FEDER-000014) for funding this Project.N/

Development of a mixed-meal that impacts carotid-body mediated cardiorespiratory and metabolic parameters - a pilot study

The carotid bodies (CB) have been recently implicated in the genesis of metabolic diseases in animal models. The CBs respond to circulating insulin to increase heart rate, respiratory rate and blood glucose levels. In humans, this mechanism is not well characterized.info:eu-repo/semantics/publishedVersio

implications for metabolic diseases

Funding: Joana F. Sacramento and Fatima O. Martins are funded by contracts from the Portuguese Foundation for Science and Technology with reference CEEC IND/02428/2018 and CEECIND/04266/2017, respectivelyNeuro-immune communication has gained enormous interest in recent years due to increasing knowledge of the way in which the brain coordinates functional alterations in inflammatory and autoimmune responses, and the mechanisms of neuron-immune cell interactions in the context of metabolic diseases such as obesity and type 2 diabetes. In this review, we will explain how this relationship between the nervous and immune system impacts the pro- and anti-inflammatory pathways with specific reference to the hypothalamus-pituitary-adrenal gland axis and the vagal reflex and will explore the possible involvement of the carotid body (CB) in the neural control of inflammation. We will also highlight the mechanisms of vagal anti-inflammatory reflex control of immunity and metabolism, and the consequences of functional disarrangement of this reflex in settlement and development of metabolic diseases, with special attention to obesity and type 2 diabetes. Additionally, the role of CB in the interplay between metabolism and immune responses will be discussed, with specific reference to the different stimuli that promote CB activation and the balance between sympathetic and parasympathetic in this context. In doing so, we clarify the multivarious neuronal reflexes that coordinate tissue-specific responses (gut, pancreas, adipose tissue and liver) critical to metabolic control, and metabolic disease settlement and development. In the final section, we will summarize how electrical modulation of the carotid sinus nerve may be utilized to adjust these reflex responses and thus control inflammation and metabolic diseases, envisioning new therapeutics horizons.publishersversionpublishe

Markers of cognitive function in individuals with metabolic disease: Morquio Syndrome and Tyrosinemia Type III

We characterized cognitive function in two metabolic diseases. MPS–IVa (mucopolysaccharidosis IVa, Morquio) and tyrosinemia type III individuals were assessed using tasks of attention, language and oculomotor function. MPS–IVa individuals were slower in visual search, but the display size effects were normal, and slowing was not due to long reaction times (ruling out slow item processing or distraction). Maintaining gaze in an oculomotor task was difficult. Results implicated sustained attention and task initiation or response processing. Shifting attention, accumulating evidence and selecting targets were unaffected. Visual search was also slowed in tyrosinemia type III, and patterns in visual search and fixation tasks pointed to sustained attention impairments, although there were differences from MPS–IVa. Language was impaired in tyrosinemia type III but not MPS–IVa. Metabolic diseases produced selective cognitive effects. Our results, incorporating new methods for developmental data and model selection, illustrate how cognitive data can contribute to understanding function in biochemical brain systems

CBmeter- a new medical device for early screening of metabolic diseases

Type 2 diabetes mellitus (T2DM) is a highly prevalent disease worldwide which is asymptomatic in about 44% of patients being critical to search for new ways of early diagnosis. Recent studies have demonstrated that the etiology of this disease may be associated with alterations in the function of the carotid body (CB), a chemosensor organ located within the bifurcation of the carotid artery. In animal models of metabolic syndrome it was observed that the CBs are overactivated, underlying diseases such as obesity, hypertension and T2DM. This discovery provided a new paradigm in the neuroendocrinology field, suggesting that diagnostic function of the CBs has predictive value for the development of metabolic diseases. Despite this fact, it is not common in clinical practice to look at the CBs as organs associated with endocrine dysfunction and we believe this is probably due to the nonexistence of a user-friendly, portable medical device that diagnosis the function of the CBs.info:eu-repo/semantics/publishedVersio

Gut microbiota and metabolic diseases

Treballs Finals de Grau de Nutrició Humana i Dietètica, Facultat de Farmàcia i Ciències de l'Alimentació, Campus de l'Alimentació de Torribera, Universitat de Barcelona. Curs: 2020-2021. Tutor: Vicenta Albarral Ávila[eng] Nowadays, it is becoming increasingly apparent that gut microbiota plays an important role in the prevention and development of metabolic diseases. Several bacterial species habit the human intestine and live in symbiosis with the host. During the last decades, abundant evidence arose confirming an active role of the microbiota in human metabolism. Hence, the disruption of the gut ecosystem might promote the development of metabolic disorders. This review aims to elucidate the current evidence regarding the mechanisms through which the gut microbiota may contribute to the protection or development of metabolic diseases. It specifically focuses on obesity, type-2 diabetes mellitus (T2DM), cardiovascular disease (CVD), and the potential interventions involving microbiota for preventing metabolic diseases.[spa] Actualmente, cada vez es más evidente el rol de la microbiota intestinal en la prevención y desarrollo de las enfermedades metabólicas. Existen una gran variedad de especies bacterianas que habitan el intestino humano y viven en simbiosis con el huésped. Durante las últimas décadas, ha surgido nueva evidencia confirmando el rol activo de la microbiota en el metabolismo humano. Por lo tanto, la disrupción del ecosistema intestinal parece que puede promover alteraciones metabólicas. El objetivo de esta revisión es elucidar la evidencia actual respecto los mecanismos a través de los cuales la microbiota puede contribuir en la protección o desarrollo de enfermedades metabólicas. Concretamente, se centra en la obesidad, la diabetes mellitus tipo 2, las enfermedades cardiovasculares y las potenciales intervenciones para prevenir estas enfermedades metabólicas a través de la microbiota

Mediterranean Diet and Metabolic Diseases

Dear Colleagues, There is increasing interest regarding the protective effect of dietary patterns on a series of metabolic diseases as compared to specific food items and nutrients, since it is well accepted that foods act synergistically. In recent years, the Mediterranean diet (MD) has gained popularity as one such dietary pattern, demonstrated to deliver many benefits according to a variety of different studies (cohort, RCT, etc.), adding to its legacy. The intention of this Special Issue is to stimulate sharing of additional clues that may further develop our understanding of the relationship between the Mediterranean diet and metabolic diseases. Another aim is to clarify potential differences in the benefits observed by different MD patterns. Moreover, as more info becomes available on the effect of MD patterns in the microbiome but also in the area of proteomics and epigenetics, relevant mechanisms and involved key mediators still need to be identified in order to provide further clarity in the description of the underlying mechanisms and the potential health outcomes occurring in response to adhering to MD. You are cordially invited to submit proposals for manuscripts that bring new elements into this interesting and promising topic. We invite clinicians and researchers to submit relevant scientific work from epidemiological or clinical studies, either original articles or reviews, to this Special Issue of Nutrients entitled “Mediterranean Diet and Metabolic Diseases”

CCN5/WISP2 and metabolic diseases.

This is the final version of the article. It first appeared from Springer via https://doi.org/10.1007/s12079-017-0437-zObesity and type 2 diabetes increase worldwide at an epidemic rate. It is expected that by the year 2030 around 500 million people will have diabetes; predominantly type 2 diabetes. The CCN family of proteins has become of interest in both metabolic and other common human diseases because of their effects on mesenchymal stem cell (MSCs) proliferation and differentiation as well as being important regulators of fibrosis. We here review current knowledge of the WNT1 inducible signaling pathway protein 2 (CCN5/WISP2). It has been shown to be an important regulator of both these processes through effects on both the canonical WNT and the TGFβ pathways. It is also under normal regulation by the adipogenic commitment factor BMP4, in contrast to conventional canonical WNT ligands, and allows MSCs to undergo normal adipose cell differentiation. CCN5/WISP2 is highly expressed in, and secreted by, MSCs and is an important regulator of MSCs growth. In a transgenic mouse model overexpressing CCN5/WISP2 in the adipose tissue, we have shown that it is secreted and circulating in the blood, the mice develop hypercellular white and brown adipose tissue, have increased lean body mass and enlarged hypercellular hearts. Obese transgenic mice had improved insulin sensitivity. Interestingly, the anti-fibrotic effect of CCN5/WISP2 is protective against heart failure by inhibition of the TGFβ pathway. Understanding how CCN5/WISP2 is regulated and signals is important and may be useful for developing new treatment strategies in obesity and metabolic diseases and it can also be a target in regenerative medicine.The studies in the authors’ laboratory are supported by grants from the People Programme (Marie Curie Actions) of the European Union's Seventh Framework Programme (FP7/2007-2013) under REA grant agreement (n° 608765), Henning and Johan Throne- Holst’s foundation for the promotion of scientific research, the Medical Research Council, Torsten Söderberg Foundation, Novo Nordisk Foundation, EFSD, Swedish Diabetes Foundation, Swedish ALF funds, Edgar Sjölund Foundation, Wilhelm and Martina Lundgren’s Foundation, the Magnus Bergvall Foundation, Lisa and Johan Grönberg Foundation, Göteborgs Diabetesförening, Sigurd and Elsa Golje’s Foundation, and the EU’s FP7 program (n°607842)

DEVELOPMENTAL ORIGINS OF METABOLIC DISEASES

Almost 2 billion adults in the world are overweight, and more than half of them are classified as obese, while nearly one-third of children globally experience poor growth and development. Given the vast amount of knowledge that has been gleaned from decades of research on growth and development, a number of questions remain as to why the world is now in the midst of a global epidemic of obesity accompanied by the “double burden of malnutrition,” where overweight coexists with underweight and micronutrient deficiencies. This challenge to the human condition can be attributed to nutritional and environmental exposures during pregnancy that may program a fetus to have a higher risk of chronic diseases in adulthood. To explore this concept, frequently called the developmental origins of health and disease (DOHaD), this review considers a host of factors and physiological mechanisms that drive a fetus or child toward a higher risk of obesity, fatty liver disease, hypertension, and/or type 2 diabetes (T2D). To that end, this review explores the epidemiology of DOHaD with discussions focused on adaptations to human energetics, placental development, dysmetabolism, and key environmental exposures that act to promote chronic diseases in adulthood. These areas are complementary and additive in understanding how providing the best conditions for optimal growth can create the best possible conditions for lifelong health. Moreover, understanding both physiological as well as epigenetic and molecular mechanisms for DOHaD is vital to most fully address the global issues of obesity and other chronic diseases