RAGE influences the development of aortic valve stenosis in mice on a high fat diet

Hofmann, Britt; Yakobus, Yuliana; Indrasari, Mailiza; Naß, Norbert; Santos, Anne Navarrete; Kraus, Frank Bernhard; Silber, Rolf-Edgar; Simm, Andreas

doi:10.1016/j.exger.2014.05.001

Cited by 22 publications

(20 citation statements)

References 31 publications

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“…Several studies imply that an HFD diet alone is not sufficient for inducing heart failure [44,70,71], while others report lipotoxic cardiomyopathy under long dietary regimens [49,50] or cardiac hypertrophy under specific FA contents of a HFD [72]. HFD treatment is also one of the established models for the induction of aortic valve disease [73][74][75]. HFD treatment altered aortic flow pattern [73].…”

Section: Discussionmentioning

confidence: 99%

The Effect of a High-Fat Diet on the Fatty Acid Composition in the Hearts of Mice

et al. 2020

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The Western diet can lead to alterations in cardiac function and increase cardiovascular risk, which can be reproduced in animal models by implementing a high-fat diet (HFD). However, the mechanism of these alterations is not fully understood and may be dependent on alterations in heart lipid composition. The aim of this study was to evaluate the effect of an HFD on the fatty acid (FA) composition of total lipids, as well as of various lipid fractions in the heart, and on heart function. C57BL/6 mice were fed an HFD or standard laboratory diet. The FA composition of chow, serum, heart and skeletal muscle tissues was measured by gas chromatography–mass spectrometry. Cardiac function was evaluated by ultrasonography. Our results showed an unexpected increase in polyunsaturated FAs (PUFAs) and a significant decrease in monounsaturated FAs (MUFAs) in the heart tissue of mice fed the HFD. For comparison, no such effects were observed in skeletal muscle or serum samples. Furthermore, we found that the largest increase in PUFAs was in the sphingolipid fraction, whereas the largest decrease in MUFAs was in the phospholipid and sphingomyelin fractions. The hearts of mice fed an HFD had an increased content of triacylglycerols. Moreover, the HFD treatment altered aortic flow pattern. We did not find significant changes in heart mass or oxidative stress markers between mice fed the HFD and standard diet. The above results suggest that alterations in FA composition in the heart may contribute to deterioration of heart function. A possible mechanism of this phenomenon is the alteration of sphingolipids and phospholipids in the fatty acid profile, which may change the physical properties of these lipids. Since phospho- and sphingolipids are the major components of cell membranes, alterations in their structures in heart cells can result in changes in cell membrane properties.

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Section: Discussionmentioning

confidence: 99%

The Effect of a High-Fat Diet on the Fatty Acid Composition in the Hearts of Mice

et al. 2020

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“…Components in these foods could possibly influence the risk of AVS by decreasing oxidation and atherogenicity of low-density lipoprotein cholesterol (antioxidant nutrients and phytochemicals in fruit, vegetables, whole grains, legumes, nuts, and olive oil) [35][36][37]; by reducing blood pressure (antioxidants and minerals in fruit, vegetables, nuts, olive oil, and low-fat dairy foods) [13,38,39] or inflammation (long-chain omega-3 polyunsaturated fatty acids in fish) [40]; by increasing blood pressure (sodium in for example processed meat) [41]; or by inducing postprandial hyperglycemia, hyperinsulinemia, and obesity (sucrose in sugar-sweetened beverages) [14]. Experimental studies in mice have shown that high-fat diets induce aortic valve disease [42,43]. The mDASH and mMED diets were inversely associated with dietary fat intake in this study but none of the dietary patterns or any of the examined food groups were associated with incidence of AVS.…”

Section: Discussionmentioning

confidence: 99%

Dietary patterns, food groups, and incidence of aortic valve stenosis: A prospective cohort study

Larsson

Wolk

Bäck

2019

International Journal of Cardiology

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Background: The role of diet in the development of aortic valve stenosis (AVS) is unknown. We therefore examined the associations of two dietary patterns, including a modified Dietary Approaches to Stop Hypertension (mDASH) diet and a modified Mediterranean (mMED) diet, and the food items included in these dietary patterns with incidence of aortic valve stenosis (AVS) in a population-based cohort study. Methods: The study cohort comprised 74,401 Swedish adults (54% men) who were free of cardiovascular disease at the time of completion of a baseline questionnaire about habitual diet and other risk factors for chronic diseases. Participants were followed-up through linkage with nationwide registers on hospitalization and causes of death. Results: During 1,132,617 person-years (mean 15.2 years) of follow-up, 1338 incident AVS cases (801 in men and 537 in women) were ascertained. We found no significant associations of the mDASH and mMED dietary patterns or the food groups and beverages included in these diets (i.e., fruit, vegetables, legumes and nuts, whole grains, fish, low-fat dairy foods, full-fat dairy foods, red and processed meat, and sweetened beverages) with risk of AVS. The hazard ratios (95% confidence interval) of AVS per one standard deviation increase in the mDASH and mMED diet scores were respectively 1.02 (0.96-1.07) and 1.00 (0.95-1.06). Conclusion: This study found no evidence that diet plays a role in the development of AVS.

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“…HFS diets can induce hyperglycemia in rodents, further linking diet-induced obesity to AGEs (Sumiyoshi et al, 2006 ). The receptor for AGEs on macrophages, called RAGE, is associated with a pro-inflammatory state, and RAGE/AGEs are reported to be involved in the onset and progression of metabolic disturbance, insulin resistance, and adipokine expression (Leuner et al, 2012 ; Hofmann et al, 2014 ). AGEs have been implicated in macrophage polarization toward M1 pro-inflammatory phenotypes, pro-inflammatory IL-6 secretion in adipose tissues, and initiating inflammatory cascades (Bopp et al, 2008 ; Frommhold et al, 2011 ; Nativel et al, 2013 ; Jin et al, 2015 ; Son et al, 2016 ) [i.e., NF-κB, p38 mitogen-activated protein kinase (MAPK)].…”

Section: Obesity and Impact On Muscle Integritymentioning

confidence: 99%

Obesity, Metabolic Syndrome, and Musculoskeletal Disease: Common Inflammatory Pathways Suggest a Central Role for Loss of Muscle Integrity

et al. 2018

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Inflammation can arise in response to a variety of stimuli, including infectious agents, tissue injury, autoimmune diseases, and obesity. Some of these responses are acute and resolve, while others become chronic and exert a sustained impact on the host, systemically, or locally. Obesity is now recognized as a chronic low-grade, systemic inflammatory state that predisposes to other chronic conditions including metabolic syndrome (MetS). Although obesity has received considerable attention regarding its pathophysiological link to chronic cardiovascular conditions and type 2 diabetes, the musculoskeletal (MSK) complications (i.e., muscle, bone, tendon, and joints) that result from obesity-associated metabolic disturbances are less frequently interrogated. As musculoskeletal diseases can lead to the worsening of MetS, this underscores the imminent need to understand the cause and effect relations between the two, and the convergence between inflammatory pathways that contribute to MSK damage. Muscle mass is a key predictor of longevity in older adults, and obesity-induced sarcopenia is a significant risk factor for adverse health outcomes. Muscle is highly plastic, undergoes regular remodeling, and is responsible for the majority of total body glucose utilization, which when impaired leads to insulin resistance. Furthermore, impaired muscle integrity, defined as persistent muscle loss, intramuscular lipid accumulation, or connective tissue deposition, is a hallmark of metabolic dysfunction. In fact, many common inflammatory pathways have been implicated in the pathogenesis of the interrelated tissues of the musculoskeletal system (e.g., tendinopathy, osteoporosis, and osteoarthritis). Despite these similarities, these diseases are rarely evaluated in a comprehensive manner. The aim of this review is to summarize the common pathways that lead to musculoskeletal damage and disease that result from and contribute to MetS. We propose the overarching hypothesis that there is a central role for muscle damage with chronic exposure to an obesity-inducing diet. The inflammatory consequence of diet and muscle dysregulation can result in dysregulated tissue repair and an imbalance toward negative adaptation, resulting in regulatory failure and other musculoskeletal tissue damage. The commonalities support the conclusion that musculoskeletal pathology with MetS should be evaluated in a comprehensive and integrated manner to understand risk for other MSK-related conditions. Implications for conservative management strategies to regulate MetS are discussed, as are future research opportunities.

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RAGE influences the development of aortic valve stenosis in mice on a high fat diet

Cited by 22 publications

References 31 publications

The Effect of a High-Fat Diet on the Fatty Acid Composition in the Hearts of Mice

The Effect of a High-Fat Diet on the Fatty Acid Composition in the Hearts of Mice

Dietary patterns, food groups, and incidence of aortic valve stenosis: A prospective cohort study

Obesity, Metabolic Syndrome, and Musculoskeletal Disease: Common Inflammatory Pathways Suggest a Central Role for Loss of Muscle Integrity

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