Incretins and Lipid Metabolism

2018 ◽  
Vol 25 (18) ◽  
pp. 2133-2139 ◽  
Author(s):  
Vasilis Tsimihodimos ◽  
Moses Elisaf

Background: Recent findings indicate that incretin hormones and incretin-based therapies may affect the metabolism of lipoproteins, although the corresponding mechanisms are not clearly defined. Objective: To summarize the available data on the mechanisms linking incretins with the characteristics of serum lipoproteins and discuss the clinical implications of these relationships. Methods: PubMed was searched using the terms “incretins”, “GLP-1”, “GIP” and “lipids”, “dyslipidemia”, “triglycerides”, “apolipoprotein B48”. All articles published in the English language until June 2016 were assessed and the relevant information is presented here. Results: GLP-1, and therapies that increase its activity, exert a beneficial effect on lipoprotein metabolism that is translated in a reduction in the fasting and postprandial concentration of triglycerides and a small improvement in the concentration and function of HDLs. In addition, a shift towards larger, less atherogenic particles usually follows the administration of GLP-1 receptor agonists. The mechanisms that underlie these changes involve a direct effect of GLP- 1 on the hepatic and intestinal production of triglyceride-rich lipoproteins, the GLP-1 induced increase in the production and function of insulin, the activation of specific areas of central nervous system as well as the increase in the peripheral utilization of triglycerides for energy production. On the other hand, GLP-2 increases the absorption of dietary fat and the production of triglyceride-rich lipoproteins while the role of GIP on lipid metabolism remains indeterminate. Conclusion: GLP-1 and incretin-based therapies favorably affect lipid metabolism. These effects may contribute to the beneficial effects of incretin-based therapies on atherosclerosis and fatty liver disease.

2020 ◽  
Vol 26 (13) ◽  
pp. 1486-1494 ◽  
Author(s):  
Melinda E. Tóth ◽  
Brigitta Dukay ◽  
Zsófia Hoyk ◽  
Miklós Sántha

Serum lipid levels are closely related to the structure and function of blood vessels. Chronic hyperlipidemia may lead to damage in both the cardio- and the cerebrovascular systems. Vascular dysfunctions, including impairments of the blood-brain barrier, are known to be associated with neurodegenerative diseases. A growing number of evidence suggests that cardiovascular risk factors, such as hyperlipidemia, may increase the likelihood of developing dementia. Due to differences in lipoprotein metabolism, wild-type mice are protected against dietinduced hypercholesterolemia, and their serum lipid profile is different from that observed in humans. Therefore, several transgenic mouse models have been established to study the role of different apolipoproteins and their receptors in lipid metabolism, as well as the complications related to pathological lipoprotein levels. This minireview focused on a transgenic mouse model overexpressing an apolipoprotein, the human ApoB-100. We discussed literature data and current advancements on the understanding of ApoB-100 induced cardio- and cerebrovascular lesions in order to demonstrate the involvement of this type of apolipoprotein in a wide range of pathologies, and a link between hyperlipidemia and neurodegeneration.


2010 ◽  
Vol 298 (1) ◽  
pp. E1-E7 ◽  
Author(s):  
Julia Kovsan ◽  
Nava Bashan ◽  
Andrew S. Greenberg ◽  
Assaf Rudich

Autophagy is a major degradative pathway(s) by which intracellular components are delivered into the lysosomes. It is largely implicated in determining cell death and survival because it eliminates unnecessary, damaged, and/or potentially harmful cellular products and organelles and is an important source for nutrients and energy production under conditions of external nutrient deficiency. As such, autophagy has been suggested to contribute to the regulation of carbohydrate and protein metabolism during fasting. Recently, three papers implicated a role for autophagy in cellular lipid metabolism as well. This Perspectives article presents these novel findings in the context of prior studies on the role of autophagy and lysosomes in metabolic and energy regulation, discusses their points of agreement and opposing propositions, and outlines key outstanding questions.


Author(s):  
Nick Ceramella

<strong><strong></strong></strong><p align="LEFT">I<span style="font-family: DejaVuSerifCondensed; font-size: small;">n the Introduction to this article, I deal with the importance of speaking one’s </span>own language as a way to assert one’s identity. Then I pass on to the evolution of the English language from its start as Old English, spoken by only a few thousand Angles and Saxons.</p><p align="LEFT"><span style="font-family: DejaVuSerifCondensed; font-size: small;">I remark how, at fi rst, it was contaminated by thousands of </span>Latin, French and Scandinavian words, of which contemporary English still bears many clear traces, but nobody has ever thought that English was ever in danger of disappearing. By contrast, in the long run, it became the mother tongue of the speakers in comparatively newly founded countries, such as the USA, Australia, and New Zealand, and owing to the spread of the British Empire, it has dramatically increased its appeal becoming the most spoken and infl uential language in the world. Thus, according to some linguists, it has led several languages virtually to the verge of disappearance. Therefore, I argue whether English has really vampirised them, or has simply contributed to make people understand each other, sometimes even in the same country where lots of diff erent tongues are spoken (e.g. Nigeria).</p><p align="LEFT">It is self-evident that English has gradually been taking the role of a common unifying factor in our globalised world. In this view, I envisage a scenario where English may even become the offi cial l anguage o f the E U with the c ontributions &amp; coming, though in varying doses, from all the speakers of the other EU languages.</p>


2001 ◽  
Vol 26 (S1) ◽  
pp. S13-S22 ◽  
Author(s):  
Henry C. Lukaski

Magnesium, zinc and chromium are mineral elements required in modest amounts for health and optimal performance. Accumulating evidence supports the hypothesis that magnesium and zinc play significant roles in promoting strength and cardiorespiratory function in healthy persons and athletes. Differences in study designs, however, limit conclusions about recommendations for intakes of magnesium and zinc needed for optimal performance and function. The role of chromium in supporting performance is not well established. There is a compelling need to confirm and extend findings of beneficial effects of magnesium and zinc function and performance of humans. Suggestions for an experimental model and specific topics for research to advance knowledge of mineral nutrition to promote attainment of genetic potential for optimal performance are provided.


2020 ◽  
Vol 11 ◽  
Author(s):  
Adam D. Langenbacher ◽  
Hirohito Shimizu ◽  
Welkin Hsu ◽  
Yali Zhao ◽  
Alexandria Borges ◽  
...  

Mitochondrial Ca2 + uptake influences energy production, cell survival, and Ca2 + signaling. The mitochondrial calcium uniporter, MCU, is the primary route for uptake of Ca2 + into the mitochondrial matrix. We have generated a zebrafish MCU mutant that survives to adulthood and exhibits dramatic cardiac phenotypes resembling cardiomyopathy and sinus arrest. MCU hearts contract weakly and have a smaller ventricle with a thin compact layer and reduced trabecular density. Damaged myofibrils and swollen mitochondria were present in the ventricles of MCU mutants, along with gene expression changes indicative of cell stress and altered cardiac structure and function. Using electrocardiography, we found that MCU hearts display conduction system defects and abnormal rhythm, with extended pauses resembling episodes of sinus arrest. Together, our findings suggest that proper mitochondrial Ca2 + homeostasis is crucial for maintaining a healthy adult heart, and establish the MCU mutant as a useful model for understanding the role of mitochondrial Ca2 + handling in adult cardiac biology.


2017 ◽  
Vol 1 ◽  
pp. maapoc.0000022 ◽  
Author(s):  
Xavier Chevalier ◽  
Thierry Conrozier

Current pharmacological therapies for osteoarthritis are symptom-focused and aimed at controlling pain. However, currently approved symptom-modifying agents do not restore the structure and function of damaged joints. Symptomatic slow-acting drugs in osteoarthritis (SySADOAs), including the sulfated glycosaminoglycan, chondroitin sulfate, have shown promising beneficial effects on the pain and other symptoms of osteoarthritis, and some may also have a positive effect on cartilage, slowing the progression of joint deterioration in osteoarthritis. A highly-purified, standardized, pharmaceutical-grade preparation of chondroitin sulfate has shown activity in osteoarthritis and has become one of the most prescribed SySADOAs. However, in many countries, formulations of chondroitin sulfate of various sources and purity are available as food supplements or nutraceuticals. As the effects of chondroitin sulfate could vary according to the characteristics of the chondroitin sulfate employed, including source, purity, or structural organization, clinical data from well-designed studies of pharmaceutical-grade chondroitin sulfate should not be extrapolated to support clinical efficacy claims of food supplements; nor should results from trials of chondroitin sulfate-containing food supplements be used to draw conclusions about the efficacy of pharmaceutical-grade chondroitin sulfate. This article reviews the evidence for the role of highly-purified pharmaceutical-grade chondroitin sulfate in the treatment of osteoarthritis and examines the efficacy and safety concerns of other formulations of chondroitin sulfate. Highly-purified pharmaceutical-grade chondroitin sulfate has mild-to-moderate efficacy in the treatment of symptomatic osteoarthritis, with clinically meaningful efficacy.


2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Dubravka Švob Štrac ◽  
Nela Pivac ◽  
Dorotea Mück-Šeler

AbstractSymptoms of cognitive dysfunction like memory loss, poor concentration, impaired learning and executive functions are characteristic features of both schizophrenia and Alzheimer’s disease (AD). The neurobiological mechanisms underlying cognition in healthy subjects and neuropsychiatric patients are not completely understood. Studies have focused on serotonin (5-hydroxytryptamine, 5-HT) as one of the possible cognitionrelated biomarkers. The aim of this review is to provide a summary of the current literature on the role of the serotonergic (5-HTergic) system in cognitive function, particularly in AD and schizophrenia.The role of the 5-HTergic system in cognition is modulated by the activity and function of 5-HT receptors (5-HTR) classified into seven groups, which differ in structure, action, and localization. Many 5-HTR are located in the regions linked to various cognitive processes. Preclinical studies using animal models of learning and memory, as well as clinicalThe current evidence implies that reduced 5-HT neurotransmission negatively influences cognitive functions and that normalization of 5-HT activity may have beneficial effects, suggesting that 5-HT and 5-HTR represent important pharmacological targets for cognition enhancement and restoration of impaired cognitive performance in neuropsychiatric disorders.


Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 173
Author(s):  
Lucia Scisciola ◽  
Rosaria Anna Fontanella ◽  
Surina ◽  
Vittoria Cataldo ◽  
Giuseppe Paolisso ◽  
...  

Sarcopenia is a geriatric syndrome characterized by the progressive degeneration of muscle mass and function, and it is associated with severe complications, which are falls, functional decline, frailty, and mortality. Sarcopenia is associated with cognitive impairment, defined as a decline in one or more cognitive domains as language, memory, reasoning, social cognition, planning, making decisions, and solving problems. Although the exact mechanism relating to sarcopenia and cognitive function has not yet been defined, several studies have shown that skeletal muscle produces and secrete molecules, called myokines, that regulate brain functions, including mood, learning, locomotor activity, and neuronal injury protection, showing the existence of muscle-brain cross-talk. Moreover, studies conducted on physical exercise supported the existence of muscle-brain cross-talk, showing how physical activity, changing myokines' circulating levels, exerts beneficial effects on the brain. The review mainly focuses on describing the role of myokines on brain function and their involvement in cognitive impairment in sarcopenia.


1997 ◽  
Vol 31 (12) ◽  
pp. 1499-1506 ◽  
Author(s):  
Judy WM Cheng ◽  
Mimi N Ngo

OBJECTIVE: To review the pathophysiology of atherosclerosis, the role of the renin—angiotensin system in atherogenesis, and studies supporting the potential beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in reducing cardiovascular events with long-term use. BACKGROUND: Through its action in converting angiotensin I to angiotensin II and by degrading bradykinin, local tissue ACE exerts many effects that can contribute to the development of atherosclerosis. Therefore, the use of ACE inhibitors can possibly result in antiatherogenic effects. Possible mechanisms for antiatherogenic effects of ACE inhibitors include: (1) reduction of blood pressure; (2) antiproliferative and antimigratory effects on vascular smooth muscle cells, neutrophils, and monocytes; (3) restoration of endothelial function; (4) stabilization of fatty plaque by preventing vasoconstriction; (5) antiplatelet effects; and (6) enhancement of endogenous fibrinolysis. DATA SOURCES: English-language clinical studies, abstracts, and review articles pertaining to the use of ACE inhibitors and atherosclerosis. STUDY SELECTION AND DATA EXTRACTION: Relevant human studies examining the role of ACE inhibitors and atherosclerosis. DATA SYNTHESIS: Studies evaluating the possible beneficial effects of ACE inhibitors in the development of atherosclerosis are reviewed and critiqued. Design of ongoing studies with clinical and surrogate end points are discussed. CONCLUSIONS: Based on current published studies, recommendations are made regarding the use of ACE inhibitors in atherosclerosis. Therapeutic monitoring parameters for efficacy and adverse effects are also reviewed.


2016 ◽  
Vol 1 (2) ◽  
pp. 102-120
Author(s):  
Herni Yuliani ◽  
Ahmad Sarbini ◽  
Herman Herman

Penelitian ini berfokus untuk mengetahui peran dan fungsi Siskohat, program Siskohat dan sosialisasi yang dilakukan oleh Siskohat dalam memberikan transparansi informasi kepada calon jemaah haji. Metode yang digunakan dalam penelitian adalah metode deskriptif. Hasil penelitian menunjukan bahwa peran Siskohat yang utama adalah sebagai pemberi informasi. Implementasi Siskohat dapat dilihat dari layanan program yang dijalankan oleh Siskohat sehingga mengsilkan informasi yang relavan sesuai dengan kebutuhan jemaah haji. Selain itu, hasil penelitian ini memperlihatkan proses transparansi yang dilakukan oleh Siskohat yang berada dibawah lembaga pemerintahan itu berarti menunjukan usaha dari pemerintah dalam upaya memberikan pelayanan optimal bagi masyarakat khusnya dalam hal ini adalah jemaah haji. This study focuses on knowing the role and function of Siskohat, the Siskohat program and the socialization carried out by Siskohat in providing information transparency to prospective pilgrims. The method used in the research is descriptive method. The results show that the main role of Siskohat is as a provider of information. The implementation of Siskohat can be seen from the program services run by Siskohat so as to produce relevant information in accordance with the needs of pilgrims. In addition, the results of this study show that the transparency process carried out by Siskohat which is under government institutions means showing the efforts of the government in an effort to provide optimal services for the community especially in this case is the pilgrims.


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