Ectopic Fat Depots and Cardiovascular Disease

Britton, Kathryn; Fox, Caroline S.

doi:10.1161/circulationaha.111.077602

Cited by 350 publications

(267 citation statements)

References 37 publications

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“…In our study, we showed that following consumption of FDW resulted in hypertrophy of central adipocytes in obese Wistar rats (Mamikutty et al 2014). Excessive fat will initially accumulate in adipose tissue, followed by the deposition in ectopic organs such as liver and heart (Britton & Fox 2011). Thus, it may lead to the complication of MetS which include non-alcoholic fatty liver disease (NAFLD).…”

Section: Discussionmentioning

confidence: 87%

Effects of 11β-Hydroxysteroid Dehydrogenase Type 1 Enzyme in the Liver in Fructose Induced Metabolic Syndrome Rat Model

Norshalizah

Zar

Suhaimi

2017

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ABSTRAK Peningkatan ekspresi dan aktiviti enzim 11β-hidroksisteroid dehidrogenase jenis 1 (11β-HSD1) di dalam sel adiposit matang menyebabkan obesiti dan sindrom metabolik. Fruktos dalam air minuman telah terbukti boleh menyebabkan sindrom metabolik pada tikus Wistar jantan. Oleh itu, kajian ini dilakukan untuk melihat Med & Health Jun 2017;12(1): 56-65 are striking resemblances between these two conditions. In contrast to Cushing's disease, plasma cortisol tends to be normal or lower in MetS. Nevertheless, rodent obesity models showed glucocorticoid plays an important role in the metabolic disease. The glucocorticoid reactivation is mediated by the enzyme known as 11β-hydroxysteroid dehydrogenase (11β-HSD). Amelung and his colleagues discovered the 11β-hydroxysteroid dehydrogenase enzyme (11β-HSD) in 1953 (Morton & Seckl 2008). This enzyme converts the inactive glucocorticoid hormone to active glucocorticoid hormone. Cortisone is an inactive form of glucocorticoid in human meanwhile ABSTRACTExcessive expression and activity of 11β-hydroxysteroid dehydrogenase enzyme type 1 (11β-HSD1) enzyme in mature adipocyte leads to obesity and metabolic syndrome. Fructose in drinking water was proven to induce metabolic syndrome in male Wistar rat. Hence, the aim of the study was to assess the effects of expression and activity of 11β-HSD1 enzyme in the liver in an established metabolic syndrome rat model induced by fructose drinking water. Twelve male Wistar rats were randomly divided into two groups: Control group, C (n=6) and Fructose drinking water 20%, F20 (n=6). The food and fluid intake were given as ad libitum for eight weeks. At the end of the experiment, the expression of 11β-HSD1 enzyme in the liver was measured by immunohistochemical staining method. The score was given according to the intensity of the staining of the granules in the hepatocyte cytoplasm which was measured using double-blinded method. Meanwhile, the activity of 11β-HSD1 enzyme in the liver was measured using ELISA technique. Following eight weeks of consumption of fructose drinking water, the F20 group showed an increased in both expression and activity of 11β-HSD1 in the liver. The obtained data clearly suggest that 11β-HSD1 enzymes in the liver may play a role in the development of metabolic syndrome and its complications in male Wistar rat.

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Section: Discussionmentioning

confidence: 87%

Effects of 11β-Hydroxysteroid Dehydrogenase Type 1 Enzyme in the Liver in Fructose Induced Metabolic Syndrome Rat Model

Norshalizah

Zar

Suhaimi

2017

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“…However, an imbalance of energy may also lead to fat accumulation in ectopic depots as visceral adipose tissue, surrounding the heart and vasculature [19,22].…”

Section: Visceral and Subcutaneous Adipose Tissuementioning

confidence: 99%

“…In many studies it has been suggested that the excess of SAT has a stronger correlation with insulin sensitivity than VAT [13]. Furthermore, Britton et al, in their review, draw our attention to the ability of subcutaneous fat to promote angiogenesis and a greater capillary network in comparison to visceral fat, which leads to a higher blood flow [22].…”

Section: Visceral and Subcutaneous Adipose Tissuementioning

confidence: 99%

Obesity phenotypes: normal-weight individuals with metabolic disorders versus metabolically healthy obese

Cembrowska

Stefańska

Odrowąż-Sypniewska

2017

Medical Research Journal

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According to recent studies, adipose tissue secretes a large number of bioactive proteins, which affect the whole body metabolism. The amount of adipose tissue is the main factor that explains metabolic disorders; however, obesity is not necessarily the result of increased body weight. Interestingly, there is a subgroup of patients with normal weight and high-risk metabolic profile. Consequently, they are significantly more likely to have metabolic disorders or cardiovascular disease (CVD). Conversely, some individuals, called metabolically healthy obese (MHO), demonstrate a favourable metabolic profile despite having high BMI index and excessive adipose tissue.The aim of this paper is to review recent studies about obesity phenotypes. Better understanding of differences between metabolically obese normal-weight (MONW) and MHO may improve the therapy and treatment of metabolic health in all obese patients. Equally importantly, it may lead to an increase in early detection of individuals with metabolic disorders, regardless of their body mass value or BMI.

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“…The function of the vasculature, particularly endothelium-dependent vasomotion, reflects quite well the overall health status of the arterial system [62] . Human obesity, characterized by accumulation of ectopic (particularly visceral) fat [63] , is associated with abnormal endothelium-dependent vasomotion and enhanced contractility to endothelin-1 [64,65] . Accordingly, a reduction in energy intake [66] or reduction in body weight [67] improves vascular function in obese patients.…”

Section: Continued Need For Disease Preventionmentioning

confidence: 99%

Childhood obesity: a life-long health risk

Barton

2012

Acta Pharmacol Sin

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Childhood obesity has become major health concern for physicians, parents, and health agencies around the world. Childhood obesity is associated with an increased risk for other diseases not only during youth but also later in life, including diabetes, arterial hypertension, coronary artery disease, and fatty liver disease. Importantly, obesity accelerates atherosclerosis progression already in children and young adults. With regard to pathophysiological changes in the vasculature, the striking similarities between physiological changes related to aging and obesity-related abnormalities are compatible with the concept that obesity causes "premature" vascular aging. This article reviews factors underlying the accelerated vascular disease development due to obesity. It also highlights the importance of recognizing childhood obesity as a disease condition and its permissive role in aggravating the development of other diseases. The importance of childhood obesity for disease susceptibility later in life, and the need for prevention and treatment are also discussed.

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Ectopic Fat Depots and Cardiovascular Disease

Cited by 350 publications

References 37 publications

Effects of 11β-Hydroxysteroid Dehydrogenase Type 1 Enzyme in the Liver in Fructose Induced Metabolic Syndrome Rat Model

Effects of 11β-Hydroxysteroid Dehydrogenase Type 1 Enzyme in the Liver in Fructose Induced Metabolic Syndrome Rat Model

Obesity phenotypes: normal-weight individuals with metabolic disorders versus metabolically healthy obese

Childhood obesity: a life-long health risk

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