The Adipose Tissue as an Endocrine Organ – A Nephrologists’ Perspective

Chudek, Jerzy; Adamczak, Marcin; Nieszporek, Teresa; Wiȩcek, Andrzej

doi:10.1159/000095320

Cited by 37 publications

(29 citation statements)

References 145 publications

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“…29,30 Cytokines produced by the adipose tissue in obesity, such as interleukin-1␤, tumor necrosis factor-␣, interleukin-6, and MCP-1, have been associated with the progression of endothelial dysfunction and renal injury. [31][32][33] We observed no effect of 10 weeks of a high-fat diet on systolic blood pressure in either the WKY rats or SHRs. However, we did observe significant albuminuria and proteinuria in the SHR groups fed the normal diet, which was further exacerbated by high fat.…”

Section: Discussioncontrasting

confidence: 50%

Endothelial Dysfunction and the Development of Renal Injury in Spontaneously Hypertensive Rats Fed a High-Fat Diet

et al. 2008

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Abstract-Obesity and hypertension have been identified as cardiovascular risk factors that contribute to the progression of end-stage renal disease. To examine the mechanisms by which a high-fat diet and hypertension contribute to endothelial dysfunction and renal injury, 8-week-old male spontaneously hypertensive rats and Wistar rats were fed a high-fat (36% fat) or a normal-fat (7% fat) diet for 10 weeks. The high-fat diet increased body weight in Wistar and hypertensive rats by 25 and 31 g, respectively. Systolic blood pressure was higher in the hypertensive rats compared with Wistar rats; however, blood pressure was unaltered by the high-fat diet. Afferent arteriole response to acetylcholine was impaired in the high-fat groups after just 3 weeks. Renal macrophage infiltration was increased in the hypertensive high-fat group compared with others, and monocyte chemoattractant protein-1 excretion was increased in both of the high-fat-fed groups. Renal PCR arrays displayed significant increases in 2 inflammatory genes in hypertensive rats fed a normal diet, 1 gene was increased in high-fat-fed Wistar rats, whereas 12 genes were increased in high-fat-fed hypertensive rats. Urinary albumin excretion was increased in the hypertensive rats compared with the Wistar rats, which was further exacerbated by the high-fat diet. Glomerular nephrin expression was reduced and desmin was increased by the high-fat diet in the hypertensive rats. Our results indicate that endothelial dysfunction precedes renal injury in normotensive and spontaneously hypertensive rats fed a high-fat diet, and hypertension with obesity induces a powerful inflammatory response and disruption of the renal filtration barrier. Key Words: obesity Ⅲ inflammation Ⅲ hypertension Ⅲ renal disease O besity and hypertension are comorbid pathological conditions that have been identified as independent risk factors for the development of endothelial dysfunction and renal disease. 1 These risk factors are increasing in prevalence at an alarming rate, with Ͼ30% of the US population classified as obese, and 1 in 3 adult Americans currently suffering from hypertension. Blood pressure is strongly correlated with body mass index, and in the Framingham Offspring Study, Յ78% of male hypertensive cases were attributable to obesity. 2 Independently obesity increases the risk for chronic kidney disease 4-fold, 3 hypertensive patients account for 25% of all chronic kidney disease patients, and obese patients with hypertension are at the greatest risk for developing chronic renal disease. 4 -6 Independently, hypertension and obesity have been linked with the development of insulin resistance, endothelial dysfunction, inflammation, and renal injury. 7,8 However, these conditions are commonly found in combination, and it is now becoming apparent that the ensuing renal injury and vascular dysfunction are results of the combination of the 2 risk factors. 9 Animal models of obesity and hypertension, such as the obese Zucker rat, have been shown to develop albuminuria, progress...

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Section: Discussioncontrasting

confidence: 50%

Endothelial Dysfunction and the Development of Renal Injury in Spontaneously Hypertensive Rats Fed a High-Fat Diet

et al. 2008

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“…Since leptin was discovered [2], white AT (WAT) was recognised as an endocrine organ and an important source of biologically active substances with a local and/ or systemic action called adipokines [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Cross-talk between adipose tissue and the HPA axis in obesity and overt hypercortisolemic states

Vicennati

Garelli

Rinaldi

et al. 2014

Hormone Molecular Biology and Clinical Investigation

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In addition to its roles in providing insulation and mechanical support, adipose tissue (AT) has been recognised as the major site for storage of surplus fuel. Since leptin was discovered, white AT (WAT) has been recognised as an endocrine organ and an important source of biologically active substances with local and/or systemic action called adipokines. The metabolic and endocrine activities of AT are under the control of several hormones: a particular role has been played by glucocorticoids (GC), which able to participate, along with other hormones, both in recruitment of progenitor cells and in differentiation and secretive activities. AT is also able to generate cortisol from cortisone through 11β-hydroxysteroid-dehydrogenase (11β-HSD). There are controversial reports in the literature, showing a hyperactivity of 11β-HSD in obesity. It has been postulated that obesity, particularly the visceral body fat distribution (V-BFD), may be considered a maladaptation to stress exposure, thus leading to hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis, and higher-than-normal cortisol levels. In this review, we will examine the cross-talk between the HPA axis and AT, their relationship under stressful events, depending on steroid hormones and different adipokine secretions.

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“…Systemic inflammation has been suggested to be a significant contributor, and is correlated with insulin resistance, wasting, oxidative stress, and endothelial dysfunction [2]. These complications are also seen in obesity, where endothelial dysfunction is one of the early stages of atherosclerosis [3]. Thus, there are many causes of atherosclerosis and, recently, the role of trace metal deficiencies on atherosclerosis process has been suggested [4,5].…”

Section: Introductionmentioning

confidence: 99%

Zinc deficiency in Chronic Kidney Disease: Is there a Relationship with Adipose Tissue and Atherosclerosis?

Lobo

Torres

Fouque

et al. 2009

Biol Trace Elem Res

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Cardiovascular complications caused by an accelerated atherosclerotic disease consist the major cause of morbidity and mortality in patients with chronic kidney disease (CKD). These patients present multiple atherosclerotic risk factors, considered traditional, as well as nontraditional risk factors such as inflammation and oxidative stress. These complications are also seen in obesity, in which endothelial dysfunction is one of the early stages of atherosclerosis. The impact of trace metal deficiencies on this process is not well studied in patients with CKD and in obese people, although the influence of trace elements depletion, particularly zinc (Zn), may have significant clinical implications. This brief review describes the functions of Zn as well as the respective role of this trace element in atherosclerosis processes, with a particular emphasis on obese patients with chronic kidney disease.

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The Adipose Tissue as an Endocrine Organ – A Nephrologists’ Perspective

Cited by 37 publications

References 145 publications

Endothelial Dysfunction and the Development of Renal Injury in Spontaneously Hypertensive Rats Fed a High-Fat Diet

Endothelial Dysfunction and the Development of Renal Injury in Spontaneously Hypertensive Rats Fed a High-Fat Diet

Cross-talk between adipose tissue and the HPA axis in obesity and overt hypercortisolemic states

Zinc deficiency in Chronic Kidney Disease: Is there a Relationship with Adipose Tissue and Atherosclerosis?

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