scholarly journals Cardiac Steatosis in HIV-A Marker or Mediator of Disease?

2018 ◽  
Vol 9 ◽  
Author(s):  
Morgan Jacob ◽  
Cameron J. Holloway
Keyword(s):  
Cardiac Steatosis

Prolonged-release pirfenidone prevents obesity-induced cardiac steatosis and fibrosis in a mouse NASH model

2020 ◽  
Author(s):  
Jorge Gutiérrez-Cuevas ◽  
Ana Sandoval-Rodríguez ◽  
Hugo Christian Monroy-Ramírez ◽  
Monica Vazquez-Del Mercado ◽  
Arturo Santos-García ◽  
...  
Keyword(s):  
Prolonged Release ◽  
Nash Model ◽  
Cardiac Steatosis

scholarly journals Systemic and heart autonomous effects of sphingosine Δ4 desaturase deficiency in lipotoxic cardiac pathophysiology

2020 ◽  
Vol 13 (8) ◽  
pp. dmm043083
Author(s):  
Stanley M. Walls ◽  
Dale A. Chatfield ◽  
Karen Ocorr ◽  
Greg L. Harris ◽  
Rolf Bodmer
Keyword(s):  
Cardiac Function ◽  
Fat Body ◽  
Model Systems ◽  
Specific Expression ◽  
Cardiac Pathology ◽  
Cardiac Chamber ◽  
Spatial Regulation ◽  
Cardiac Pathophysiology ◽  
Cardiac Steatosis ◽  
Fractional Shortening

ABSTRACTLipotoxic cardiomyopathy (LCM) is characterized by cardiac steatosis, including the accumulation of fatty acids, triglycerides and ceramides. Model systems have shown the inhibition of ceramide biosynthesis to antagonize obesity and improve insulin sensitivity. Sphingosine Δ4 desaturase (encoded by ifc in Drosophila melanogaster) enzymatically converts dihydroceramide into ceramide. Here, we examine ifc mutants to study the effects of desaturase deficiency on cardiac function in Drosophila. Interestingly, ifc mutants exhibited classic hallmarks of LCM: cardiac chamber dilation, contractile defects and loss of fractional shortening. This outcome was phenocopied in global ifc RNAi-mediated knockdown flies. Surprisingly, cardiac-specific ifc knockdown flies exhibited cardiac chamber restriction with no contractile defects, suggesting heart autonomous and systemic roles for ifc activity in cardiac function. Next, we demonstrated that ifc mutants exhibit suppressed Sphingosine kinase 1 (Sk1) expression. Ectopic overexpression of Sk1 was sufficient to prevent cardiac chamber dilation and loss of fractional shortening in ifc mutants. Partial rescue was also observed with cardiac- and fat-body-specific Sk1 overexpression. Finally, we showed that cardiac-specific expression of Drosophila inhibitor of apoptosis (dIAP) also prevented cardiac dysfunction in ifc mutants, suggesting a role for caspase activity in the observed cardiac pathology. Collectively, we show that spatial regulation of sphingosine Δ4 desaturase activity differentially affects cardiac function in heart autonomous and systemic mechanisms through tissue interplay.

scholarly journals Cardiac Steatosis in Diabetes Mellitus

Circulation ◽  
2007 ◽  
Vol 116 (10) ◽  
pp. 1170-1175 ◽  
Author(s):  
Jonathan M. McGavock ◽  
Ildiko Lingvay ◽  
Ivana Zib ◽  
Tommy Tillery ◽  
Naomi Salas ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cardiac Steatosis

P3478Glucose-dependent insulinotropic peptide is essential for maintenance of cardiac lipid metabolism via FGF21-dependent pathway

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
Y Remina ◽  
Y Kureishi Bando ◽  
R Ozaki ◽  
T Kamihara ◽  
K Nishimura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Left Ventricular ◽  
Insulin Biosynthesis ◽  
Fibroblast Growth Factor 21 ◽  
Tunel Staining ◽  
Triglyceride Accumulation ◽  
Sensitive Organ ◽  
Cardiac Steatosis ◽  
Insulinotropic Peptide ◽  
And Oxidative Stress

Abstract Background/Introduction Incretin hormones, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are secreted from the small intestine and emerged as important participants in glucose homeostasis that involves in the pathogenesis of type 2 diabetes (T2D). stimulate glucose-dependent insulin biosynthesis. Emerging data suggest important extrapancreatic functions for GLP-1 on cardiovascular system. However, limited evidence has been emerged whether GIP may play any pathophysiological role in heart. GIP promotes insulin secretion leading to augment insulin-induced lipogenesis. Recent research has highlighted the relevance of the GIP/GIPR axis in principal insulin-sensitive organs such as adipose tissue. Heart is another insulin-sensitive organ in which insulin promotes hypertrophy of myocardium presumably via activation of Akt pathway. In T2DM, ectopic accumulation of lipid and fat to myocardium that is known as “cardiac steatosis”; however, it remains uncertain whether the GIP/insulin axis may modulate cardiac steatosis observed in T2DM. Purpose To elucidate that physiological GIP may play a regulatory role in cardiac pathophysiology. Methods We employed mouse model of GIPR deficiency (GIPR-KO) that was generated by lacking the GIPR gene (GIPR), by replacing exons 4 and 5 of GIPR with the PGK-neo cassette. Cardiac evaluation of GIPR-KO was performed at the age of 6 week-old (w/o), 10 w/o, 23 w/o, and 53 w/o. Results GIPR deficient mice (GIPR-KO) exhibited normoglycemia, but their circulating free acid level and ketone level were elevated. Interestingly, GIPR-KO at younger age (6-week-old and 10-week old) exhibited normal left-ventricular (LV) function, however, older mice aged older than 20-week-old exhibited significant systolic left-ventricular dysfunction (FS (%) 55.2±1.9 for Wild-type, 32.1±2.6 for 23-w/o-GIPR-KO, 28.5±2.6 for 56-w/o-GIPR-KO, P<0.01). Histological analysis revealed that cardiomyocyte size was decreased and capillary density was increased in GIPR-KO. Interestingly, TUNEL staining revealed that there was no increase in cardiac apoptosis in GIPR-KO. In contrast, GIPR-KO exhibited increase in cardiac fibrosis (Picro-sirius staining) and oxidative stress (DHE staining). Myocardial triglyceride accumulation was decreased in GIPR-KO heart. QPCR analysis revealed GIPR-KO heart exhibited increase in BNP level and decline in fibroblast growth factor 21 (FGF-21), an hormonal activator for energy expenditure in adipocyte. GIP augmented FGF-21 expression in cardiomyocytes via PPARalfa. Conclusion Loss of GIP signaling caused impaired fatty acid metabolism in heart via impairment of FGF21 pathway and oxidative stress, leading to an age-dependent progression of cardiac dysfunction.

GLP-1 analog liraglutide protects against cardiac steatosis, oxidative stress and apoptosis in streptozotocin-induced diabetic rats

2015 ◽  
Vol 240 (1) ◽  
pp. 250-259 ◽  
Author(s):  
Tomoaki Inoue ◽  
Toyoshi Inoguchi ◽  
Noriyuki Sonoda ◽  
Hari Hendarto ◽  
Hiroaki Makimura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Rats ◽  
Cardiac Steatosis

Dietary saturated fatty acids aggravate pressure overload-induced cardiomyopathy in mice in the absence of cardiac steatosis

2016 ◽  
Vol 252 ◽  
pp. e119
Author(s):  
I. Muthuramu ◽  
R. Amin ◽  
N. Singh ◽  
A. Postnov ◽  
O. Gheysens ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Saturated Fatty Acids ◽  
Pressure Overload ◽  
Cardiac Steatosis

scholarly journals Coconut Oil Aggravates Pressure Overload-Induced Cardiomyopathy without Inducing Obesity, Systemic Insulin Resistance, or Cardiac Steatosis

2017 ◽  
Vol 18 (7) ◽  
pp. 1565 ◽  
Author(s):  
Ilayaraja Muthuramu ◽  
Ruhul Amin ◽  
Andrey Postnov ◽  
Mudit Mishra ◽  
Frank Jacobs ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Pressure Overload ◽  
Coconut Oil ◽  
Systemic Insulin Resistance ◽  
Cardiac Steatosis

scholarly journals Myocardial Fat Accumulation Is Independent of Measures of Insulin Sensitivity

2015 ◽  
Vol 100 (8) ◽  
pp. 3060-3068 ◽  
Author(s):  
Ranganath Muniyappa ◽  
Radwa Noureldin ◽  
Ronald Ouwerkerk ◽  
Elizabeth Y. Liu ◽  
Ritu Madan ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Serum Triglyceride ◽  
Tolerance Test ◽  
Cross Sectional Study ◽  
Glucose Disposal ◽  
Sensitivity Index ◽  
Cross Sectional ◽  
Peripheral Insulin Sensitivity ◽  
Cardiac Steatosis ◽  
Myocardial Steatosis

Background: Myocardial steatosis, an independent predictor of diastolic dysfunction, is frequently present in type 2 diabetes mellitus. High free fatty acid flux, hyperglycemia, and hyperinsulinemia may play a role in myocardial steatosis. There are no prior studies examining the relationship between insulin sensitivity (antilipolytic and glucose disposal actions of insulin) and cardiac steatosis. Objective: Using a cross-sectional study design of individuals with and without metabolic syndrome (MetSyn), we examined the relationships between cardiac steatosis and the sensitivity of the antilipolytic and glucose disposal actions of insulin. Methods: Pericardial fat (PF) volume, intramyocardial and hepatic fat (MF and HF) content, visceral fat (VF) and sc fat content were assessed by magnetic resonance imaging in 77 subjects (49 without MetSyn and 28 with MetSyn). In a subset of the larger cohort (n = 52), peripheral insulin sensitivity index (SI) and adipocyte insulin sensitivity (Adipo-SI) were determined from an insulin-modified frequently sampled iv glucose tolerance test. The Quantitative Insulin Sensitivity Check Index was used as a surrogate for hepatic insulin sensitivity. Results: Individuals with the MetSyn had significantly higher body mass index, total body fat, and MF, PF, HF, and VF content. HF and VF, but not MF, were negatively correlated with the Quantitative Insulin Sensitivity Check Index, Adipo-SI, and SI. Stepwise regression revealed that waist circumference and serum triglyceride levels independently predicted MF and PF, respectively. Adipo-SI and serum triglyceride levels independently predict HF. Conclusion: Myocardial steatosis is unrelated to hepatic, adipocyte, or peripheral insulin sensitivity. Although it is frequently observed in insulin-resistant subjects, further studies are necessary to identify and delineate pathogenic mechanisms that differentially affect cardiac and hepatic steatosis.

scholarly journals A Diet Rich in Medium-Chain Fatty Acids Improves Systolic Function and Alters the Lipidomic Profile in Patients With Type 2 Diabetes: A Pilot Study

2016 ◽  
Vol 101 (2) ◽  
pp. 504-512 ◽  
Author(s):  
Sophia Airhart ◽  
W. Todd Cade ◽  
Hui Jiang ◽  
Andrew R. Coggan ◽  
Susan B. Racette ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Fatty Acids ◽  
Animal Models ◽  
Outcome Measures ◽  
Medium Chain ◽  
Medium Chain Fatty Acids ◽  
Cardiac Steatosis ◽  
And Function ◽  
Chain Fatty Acids

Abstract Context: Excessive cardiac long-chain fatty acid (LCFA) metabolism/storage causes cardiomyopathy in animal models of type 2 diabetes. Medium-chain fatty acids (MCFAs) are absorbed and oxidized efficiently. Data in animal models of diabetes suggest MCFAs may benefit the heart. Objective: Our objective was to test the effects of an MCFA-rich diet vs an LCFA-rich diet on plasma lipids, cardiac steatosis, and function in patients with type 2 diabetes. Design: This was a double-blind, randomized, 2-week matched-feeding study. Setting: The study included ambulatory patients in the general community. Patients: Sixteen patients, ages 37–65 years, with type 2 diabetes, an ejection fraction greater than 45%, and no other systemic disease were included. Intervention: Fourteen days of a diet rich in MCFAs or LCFAs, containing 38% as fat in total, was undertaken. Main Outcome Measures: Cardiac steatosis and function were the main outcome measures, with lipidomic changes considered a secondary outcome. Results: The relatively load-independent measure of cardiac contractility, S′, improved in the MCFA group (P &lt; .05). Weight-adjusted stroke volume and cardiac output decreased in the LCFA group (both P &lt; .05). The MCFA, but not the LCFA, diet decreased several plasma sphingolipids, ceramide, and acylcarnitines implicated in diabetic cardiomyopathy, and changes in several sphingolipids correlated with improved fasting insulins. Conclusions: Although a diet high in MCFAs does not change cardiac steatosis, our findings suggest that the MCFA-rich diet alters the plasma lipidome and may benefit or at least not harm cardiac function and fasting insulin levels in humans with type 2 diabetes. Larger, long-term studies are needed to further evaluate these effects in less-controlled settings.

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