177,090 research outputs found
Sugars, exercise and health
No full textBackground: There is a direct link between a variety of addictions and mood states to which exercise could be relieving. Sugar addiction has been recently counted as another binge/compulsive/addictive eating behavior, differently induced, leading to a high-significant health problem. Regularly exercising at moderate intensity has been shown to efficiently and positively impact upon physiological imbalances caused by several morbid conditions, including affective disorders. Even in a wider set of physchiatric diseases, physical exercise has been prescribed as a complementary therapeutic strategy. Method: A comprehensive literature search was carried out in the Cochrane Library and MEDLINE databases (search terms: sugar addiction, food craving, exercise therapy, training, physical fitness, physical activity, rehabilitation and aerobic). Results: Seeking high-sugar diets, also in a reward- or craving-addiction fashion, can generate drastic metabolic derangements, often interpolated with affective disorders, for which exercise may represent a valuable, universal, non-pharmachological barrier. Limitations: More research in humans is needed to confirm potential exercise-mechanisms that may break the bond between sugar over-consumption and affective disorders. Conclusions: The purpose of this review is to address the importance of physical exercise in reversing the gloomy scenario of unhealthy diets and sedentary lifestyles in our modern society
Treatment of Diabetes with Lifestyle Changes: Physical Activity
No full textLifestyle improvements, like dietary changes and increased physical activity, are typically advocated for the cure, prevention, and reversion of several metabolic diseases, including diabetes mellitus. The non-pharmacological low-cost nature, along with the health-related benefits, increases the therapeutical appeal of regular physical activity. In the comprehensive approach of diabetes management, regular physical activity reduces risk of many diseases to which individuals with diabetes, particularly those with type 2 diabetes mellitus, are predisposed: hypertension, coronary heart diseases, and obesity.
The present chapter covers how exercise can facilitate optimal glucose control and lipid levels, assist in weight management, and prevent exacerbation of underlying diabetes-complications, moving medicine forward, far beyond the simplistic motto of “exercise more.
Exercise has the guts: how physical activity may positively modulate gut microbiota in chronic and immune-based diseases
No full textLimited animal and human research findings suggests that exercise might have a beneficial role for health gut. Cardiorespiratory fitness correlates with health-associated gut parameters such as taxonomic diversity and richness. Physical exercise may augment intestinal microbial diversity through several mechanisms including promotion of an anti-inflammatory state. Disease-associated microbial functions were linked to distinct taxa in previous studies of familial type 1 diabetes mellitus (T1D). An integrated multi-approach in the study of T1D, including physical exercise, is advocated. The present review explores how exercise might modulate gut microbiota and microbiome characteristics in chronic and immune-based diseases, given the demonstrated relationship between gut function and human health
L-Carnitine attenuates fibrosis and inflammation in C57BL/6 mice with dietary-induced steatohepatitis
No full textNonalcoholic steatohepatitis (NASH) represents an advanced stage of fatty liver disease developed in the absence of alcohol abuse and its prevalence is increasing in western countries in parallel with Type 2 Diabetes and metabolic syndrome incidence.
NASH is a strong marker of cardiovascular risk and in the last few decades it has become evident that there is a mutual interaction between heart and liver influencing their individual functions.
In effect, NASH characterized by excess of intracellular fatty acids, severe inflammatory and fibrotic state, plays a critical role in two principal tissues: liver and heart.
Several studies have examined the effectiveness of L-Carnitine (LC) in liver function and have recognized LC as a nutritional supplementation in cardiovascular disease.
The present study was designed to investigate the effects of LC administration on liver and heart function and morphology in mice models of steatohepatitis, induced by a methionine-choline deficient diet (MCD).
C57BL/6 mice male (n=18, age:12 weeks) were divided in 3 different groups: control group (CONTR) were fed for 6 weeks with a normal diet while both MCD and LC groups received MCD diet. From the 4th week LC group received MCD diet enriched with 200mg/kg/die LC (drinking water). The results showed that there are no significant differences in body weight between MCD and LC mice groups, while, as expected, there is a significant weight loss in MCD and LC groups in respect with CONTR. Furthermore, insulin sensitivity (IPGTT test) and GLUT4 protein content showed no differences between groups.
Tissues fat deposition, inflammatory infiltration and fibrosis were, then, investigated. Different histopathology staining methods showed that LC significantly reduces fat accumulation. Immunofluorescence assay revealed an important downregulation of the two markers of tissue fibrosis: alpha smooth muscle actin protein level and Kruppel-like factor (KLF15). To clarify LC cellular mechanisms in counteracting inflammatory liver state, we evaluated NFκB pathway and PPARγ: our results indicated that NFkB increase, caused by MCD diet, was markedly attenuated by LC. In addition, LC significantly stimulates Ca2+/calmodulin-dependent kinases II activity, suggesting that LC could ameliorate mitochondrial function. Noteworthy, we observed LC actives ERKs pathway, which is correlated with a reduction of oxidative stress and hepatotoxicity.
In parallel, to investigate LC anti-inflammatory and fibrotic role in heart, we studied STAT-3 activation: LC significantly decreases STAT 3 activation observed in MCD heart. This data is in accordance with the reduction of Calcium signaling in LC heart compared to MCD.
In conclusion, LC appear to exert different beneficial actions on the liver-heart axis counteracting steatohepa¬titis. LC supplementation may be used in order to prevent disease progression in these analyzed tissues, inhibiting the inflammation and fibrotic pathways
Small wind turbines applications in seaports: cost analysis and market potential in Italy
No full textDevelop a Sustainable Product through Open Innovation: How to Make it the Standard Approach
No full textMay the force be with you: why resistance training is essential for subjects with type 2 diabetes mellitus without complications
No full textPhysical activity, together with diet and pharmacological therapy, represents one of the three cornerstones in type 2 diabetes mellitus treatment and care. The therapeutic appeal of regular physical activity stems from: (i) its non-pharmacological nature; (ii) its beneficial effects on the metabolic risk factors associated with diabetes complications; (iii) its low costs. Evidence accumulated in the last years suggests that aerobic training—endurance training—constitutes a safe modality of intervention, achievable, and effective in diabetes treatment, whenever it is not limited by comorbidities. Aerobic training exerts insulin-mimetic effects and has been shown to lower mortality risk too. Anaerobic, intense physical activity, such as that of strength or power sports disciplines, is not univocally recognized as safe and simple to realize, however, it is important in stimulating energy and glucose metabolism. According to recent evidence, high-intensity training may be prescribed even in the face of cardiovascular diseases, peripheral vascular disease, or osteoarthritis. Some studies have shown resistance training to be more efficient than aerobic exercise in improving glycemic control. This review explores the most up-to-date indications emerging from literature in support of the beneficial effects of strength stimulation and resistance training in patients with type 2 diabetes without complications
Appropriate Similarity Measures for Author Cocitation Analysis
No full textWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
data set from Mollica G, Senesi P, Codella R, Vacante F, Montesano A, Luzi L, Terruzzi I. L-carnitine supplementation attenuates NAFLD progression and cardiac dysfunction in a mouse model fed with methionine and choline-deficient diet. Dig Liver Dis. 2020 Mar;52(3):314-323. doi: 10.1016/j.dld.2019.09.002. Epub 2019 Oct 10. PMID: 31607566.
No full text<p>data set from Mollica G, Senesi P, Codella R, Vacante F, Montesano A, Luzi L, Terruzzi I. L-carnitine supplementation attenuates NAFLD progression and cardiac dysfunction in a mouse model fed with methionine and choline-deficient diet. Dig Liver Dis. 2020 Mar;52(3):314-323. doi: 10.1016/j.dld.2019.09.002. Epub 2019 Oct 10. PMID: 31607566.</p>
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<p>Non-alcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disorder. NAFLD, associated lipotoxicity, fibrosis, oxidative stress, and altered mitochondrial metabolism, is responsible for systemic inflammation, which contributes to organ dysfunction in extrahepatic tissues, including the heart. We investigated the ability of L-carnitine (LC) to oppose the pathogenic mechanisms underlying NAFLD progression and associated heart dysfunction, in a mouse model of methionine-choline-deficient diet (MCDD). Mice were divided into three groups: namely, the control group (CONTR) fed with a regular diet and two groups fed with MCDD for 6 weeks. In the last 3 weeks, one of the MCDD groups received LC (200 mg/kg each day) through drinking water (MCDD + LC). The hepatic lipid accumulation and oxidative stress decreased after LC supplementation, which also reduced hepatic fibrosis via modulation of α-smooth muscle actin (αSMA), peroxisome-activated receptor gamma (PPARγ), and nuclear factor kappa B (NfƙB) expression. LC ameliorated systemic inflammation, mitigated cardiac reactive oxygen species (ROS) production, and prevented fibrosis progression by acting on signal transducer and activator of transcription 3 (STAT3), extracellular signal-regulated kinase 1-2 (ERK1-2), and αSMA. This study confirms the existence of a relationship between fatty liver disease and cardiac abnormalities and highlights the role of LC in controlling liver oxidative stress, steatosis, fibrosis, and NAFLD-associated cardiac dysfunction.</p>
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Betaine supplement enhances skeletal muscle differentiation in murine myoblasts via IGF-1 signaling activation
No full textBackground: Betaine (BET) is a component of many foods, including spinach and wheat. It is an essential osmolyte and a source of methyl groups. Recent studies have hypothesized that BET might play a role in athletic performance. However, BET effects on skeletal muscle differentiation and hypertrophy are still poorly understood.Methods: We examined BET action on neo myotubes maturation and on differentiation process, using C2C12 murine myoblastic cells. We used RT2-PCR array, Western blot and immunofluorescence analysis to study the BET effects on morphological features of C2C12 and on signaling pathways involved in muscle differentiation and hypertrophy.Results: We performed a dose-response study, establishing that 10 mM BET was the dose able to stimulate morphological changes and hypertrophic process in neo myotubes. RT2-PCR array methodology was used to identify the expression profile of genes encoding proteins involved in IGF-1 pathway. A dose of 10 mM BET was found to promote IGF-1 receptor (IGF-1 R) expression. Western blot and immunofluorescence analysis, performed in neo myotubes, pointed out that 10 mM BET improved IGF-1 signaling, synthesis of Myosin Heavy Chain (MyHC) and neo myotubes length.In addition, we investigated BET role on myoblasts proliferation and differentiation. During proliferation, BET did not modify C2C12 proliferative rate, but promoted myogenic induction, enhancing MyoD protein content and cellular elongation. During differentiation, BET caused an increase of muscle-specific markers and IGF-1 R protein levels.Conclusions: Our findings provide the first evidence that BET could promote muscle fibers differentiation and increase myotubes size by IGF-1 pathway activation, suggesting that BET might represent a possible new drug/integrator strategy, not only in sport performance but also in clinical conditions characterized by muscle function impairment
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