Molecular Links Between Obesity and Cardiovascular Disease

Sorisky, Alexander

doi:10.1097/00045391-200211000-00010

Cited by 18 publications

(14 citation statements)

References 50 publications

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“…Age-related neuronal loss appears to be accelerated by a number of vascular factors that increase ischemia. 35,36 Obesity has been related to ischemia, in addition to a variety of vascular pathologies that are also potentially related to atrophy, including carotid artery wall thickening, 19 vascular and coronary endothelial dysfunction, 18,20,37,38 peripheral resistance, arterial stiffness, 39 ventricular hypertrophy, and increased sympathetic activity, intravascular volume, cardiac output, lipid levels, 40 and platelet aggregation. 39,41 Third, obesity may increase cortisol secretion, 42 which may lead to atrophy.…”

Section: Resultsmentioning

confidence: 99%

“…7 In epidemiologic studies, cerebral atrophy has been related to a variety of vascular factors such as hypertension, [11][12][13] declining blood pressure over time, 14 cerebrovascular and cardiovascular disease, 12 diabetes, 15 smoking, 11 and high alcohol intake. 16,17 As a major vascular risk factor, overweight may trigger cerebral atrophy directly [18][19][20] or secondarily by leading to or exacerbating the aforementioned vascular factors such as high blood pressure.…”

mentioning

confidence: 99%

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A 24-year follow-up of body mass index and cerebral atrophy

Gustafson

Lissner²,

Bengtsson³

et al. 2004

Neurology

295

231

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

A 24-year follow-up of body mass index and cerebral atrophy

Gustafson

Lissner²,

Bengtsson³

et al. 2004

Neurology

295

231

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show abstract

“…Activation of a TNF -responsive serine kinase causes serine-phosphorilation of insulin receptor substrate (IRS)-1, resulting in a reduction of insulin signaling. Serinephosphorilated IRS-1 is less effective in activating phosphoinositide 3-kinase (PI3K), involved in insulindetermined lipolysis suppression [39]. It has been previously suggested that TNF may also have paracrine actions, affecting insulin-stimulated glucose uptake at the skeletal muscle [39].…”

Section: Tumor Necrosis Factor Alpha (Tnf )mentioning

confidence: 99%

The New Adipose Tissue and Adipocytokines

Bulcão¹,

Ferreira²,

Giuffrida³

et al. 2006

CDR

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Obesity is a well-known risk factor for the development of insulin resistance, type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease. Rather than the total amount of fat, central distribution of adipose tissue is very important in the pathophysiology of this constellation of abnormalities termed metabolic syndrome. Adipose tissue, regarded only as an energy storage organ until the last decade, is now known as the biggest endocrine organ of the human body. This tissue secretes a number of substances--adipocytokines--with multiple functions in metabolic profile and immunological process. Therefore, excessive fat mass may trigger metabolic and hemostatic disturbances as well as CVD. Adipocytokines may act locally or distally as inflammatory, immune or hormonal signalers. In this review we discuss visceral obesity, the potential mechanisms by which it would be related to insulin resistance, methods for its assessment and focus on the main adipocytokines expressed and secreted by the adipose tissue. Particularly, we review the role of adiponectin, leptin, resistin, angiotensinogen, TNF-alpha, and PAI-1, describing their impact on insulin resistance and cardiovascular risk, based on more recent findings in this area.

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“…These elevated levels may in turn contribute directly or indirectly to the increased incidence of cardiovascular diseases (4). A significant correlation has been found between body mass index and circulating levels of C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor ␣ (TNF ␣ ) (5-7).…”

mentioning

confidence: 99%

Characterization of the long pentraxin PTX3 as a TNFα-induced secreted protein of adipose cells

Abderrahim-Ferkoune

Bézy

Chiellini

et al. 2003

Journal of Lipid Research

126

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Exposure of preadipocytes to long-chain fatty acids induces the expression of several markers of adipocyte differentiation. In an attempt to identify novel genes and proteins that are regulated by fatty acids in preadipocytes, we performed a substractive hybridization screening and identified PTX3, a protein of the pentraxin family. PTX3 mRNA expression is transient during adipocyte differentiation of clonal cell lines and is absent in fully differentiated cells. Stable overexpression of PTX3 in preadipocytes has no effect on adipocyte differentiation. In line with this, PTX3 mRNA is expressed in the stromal-vascular fraction of adipose tissue, but not in the adipocyte fraction; however, in 3T3-F442A adipocytes, the PTX3 gene can be reinduced by tumor necrosis factor ␣ (TNF ␣ ) in a dose-dependent manner. This effect is accompanied by PTX3 protein secretion from both 3T3-F442A adipocytes and explants of mouse adipose tissue. PTX3 mRNA levels are found to be higher in adipose tissue of genetically obese mice versus control mice, consistent with their increased TNF ␣ levels. In conclusion, PTX3 appears as a TNF ␣ -induced protein that provides a new link between chronic low-level inflammatory state and obesity. -Abderrahim-Ferkoune, A., O.

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Molecular Links Between Obesity and Cardiovascular Disease

Cited by 18 publications

References 50 publications

A 24-year follow-up of body mass index and cerebral atrophy

A 24-year follow-up of body mass index and cerebral atrophy

The New Adipose Tissue and Adipocytokines

Characterization of the long pentraxin PTX3 as a TNFα-induced secreted protein of adipose cells

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