scholarly journals From Obesity to Chronic Kidney Disease: How Can Adipose Tissue Affect Renal Function?

Nephron ◽  
2021 ◽  
pp. 1-5
Author(s):  
Marina Martin-Taboada ◽  
Rocío Vila-Bedmar ◽  
Gema Medina-Gómez

Obesity is directly associated with an increased risk of developing CKD, regardless of other comorbid conditions. Although the molecular mechanisms that link both diseases are not well established, the role of adipose tissue (AT) is becoming increasingly important in obesity-associated kidney damage. In the context of obesity, lipotoxicity and the alteration of AT secretion profile promote inflammation, oxidative stress, and fibrosis in the kidney, which ultimately leads to impaired renal function. Different studies have highlighted the importance of body weight loss in the improvement of renal function markers. In this regard, bariatric surgery, rather than low-calorie diets, has been accepted as the most effective option to lose weight. In fact, a significant reduction in proteinuria and hyperfiltration has been observed in association with surgically induced weight loss. Detection of early signs of kidney dysfunction in patients with obesity has not been accomplished yet, though. Therefore, understanding the harmful effects within the adipo-renal axis is essential to prevent the progression to the irreversible renal insufficiency. MicroRNAs have recently been described as important modulators of normal kidney function. Some of these microRNAs could be potential early markers of kidney damage, which would help with the diagnosis and the prevention of CKD.

Genes ◽  
2018 ◽  
Vol 9 (11) ◽  
pp. 525 ◽  
Author(s):  
Samar Tareen ◽  
Michiel Adriaens ◽  
Ilja Arts ◽  
Theo de Kok ◽  
Roel Vink ◽  
...  

Obesity is a global epidemic identified as a major risk factor for multiple chronic diseases and, consequently, diet-induced weight loss is used to counter obesity. The adipose tissue is the primary tissue affected in diet-induced weight loss, yet the underlying molecular mechanisms and changes are not completely deciphered. In this study, we present a network biology analysis workflow which enables the profiling of the cellular processes affected by weight loss in the subcutaneous adipose tissue. Time series gene expression data from a dietary intervention dataset with two diets was analysed. Differentially expressed genes were used to generate co-expression networks using a method that capitalises on the repeat measurements in the data and finds correlations between gene expression changes over time. Using the network analysis tool Cytoscape, an overlap network of conserved components in the co-expression networks was constructed, clustered on topology to find densely correlated genes, and analysed using Gene Ontology enrichment analysis. We found five clusters involved in key metabolic processes, but also adipose tissue development and tissue remodelling processes were enriched. In conclusion, we present a flexible network biology workflow for finding important processes and relevant genes associated with weight loss, using a time series co-expression network approach that is robust towards the high inter-individual variation in humans.


Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1686 ◽  
Author(s):  
Ryan Kolb ◽  
Weizhou Zhang

Obesity is associated with an increased risk of estrogen receptor-positive breast cancer in postmenopausal women and a worse prognosis for all major breast cancer subtypes regardless of menopausal status. While the link between obesity and the pathogenesis of breast cancer is clear, the molecular mechanism of this association is not completely understood due to the complexity of both obesity and breast cancer. The aim of this review is to highlight the association between obesity and breast cancer and discuss the literature, which indicates that this association is due to chronic adipose tissue inflammation. We will discuss the epidemiological data for the association between breast cancer incidence and progression as well as the potential molecular mechanisms for this association. We will focus on the role of inflammation within the adipose tissue during the pathogenesis of breast cancer. A better understanding of how obesity and adipose tissue inflammation affects the pathogenesis of breast cancer will lead to new strategies to reduce breast cancer risk and improve patient outcomes for obese patients.


1958 ◽  
Vol 13 (1) ◽  
pp. 129-134 ◽  
Author(s):  
Cecil Entenman ◽  
William H. Goldwater ◽  
Nell S. Ayres ◽  
Albert R. Behnke

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3195
Author(s):  
Yo-Han Han ◽  
Jeong-Geon Mun ◽  
Hee Dong Jeon ◽  
Dae Hwan Yoon ◽  
Byung-Min Choi ◽  
...  

Background: Cachexia induced by cancer is a systemic wasting syndrome and it accompanies continuous body weight loss with the exhaustion of skeletal muscle and adipose tissue. Cancer cachexia is not only a problem in itself, but it also reduces the effectiveness of treatments and deteriorates quality of life. However, effective treatments have not been found yet. Although Arctii Fructus (AF) has been studied about several pharmacological effects, there were no reports on its use in cancer cachexia. Methods: To induce cancer cachexia in mice, we inoculated CT-26 cells to BALB/c mice through subcutaneous injection and intraperitoneal injection. To mimic cancer cachexia in vitro, we used conditioned media (CM), which was CT-26 colon cancer cells cultured medium. Results: In in vivo experiments, AF suppressed expression of interleukin (IL)-6 and atrophy of skeletal muscle and adipose tissue. As a result, the administration of AF decreased mortality by preventing weight loss. In adipose tissue, AF decreased expression of uncoupling protein 1 (UCP1) by restoring AMP-activated protein kinase (AMPK) activation. In in vitro model, CM increased muscle degradation factors and decreased adipocytes differentiation factors. However, these tendencies were ameliorated by AF treatment in C2C12 myoblasts and 3T3-L1 cells. Conclusion: Taken together, our study demonstrated that AF could be a therapeutic supplement for patients suffering from cancer cachexia.


2011 ◽  
Vol 1 (S1) ◽  
Author(s):  
Denise Carmona Cara ◽  
Luana PA Dourado ◽  
Mria LM Noviello ◽  
Debora M Alvarenga ◽  
Gustavo B Menezes ◽  
...  

2021 ◽  
Author(s):  
Irving L. M. H. Aye ◽  
Fredrick J. Rosario ◽  
Anita Kramer ◽  
Oddrun Kristiansen ◽  
Trond M. Michelsen ◽  
...  

ABSTRACTIn pregnancy, adiponectin serves as an endocrine link between maternal adipose tissue, placental function and fetal growth, with low adiponectin promoting placental function and fetal growth. Circulating adiponectin levels are decreased in obese pregnant women and in gestational diabetes, which is believed to contribute to the insulin resistance and increased risk of fetal overgrowth associated with these conditions. However, the molecular mechanisms governing adiponectin secretion from maternal adipose tissues in pregnancy are poorly understood. Using visceral adipose tissue from lean and obese pregnant mice, we show that obesity in pregnancy is associated with adipose tissue inflammation, ER stress, insulin resistance, increased adiponectin ubiquitination and decreased total abundance of adiponectin. Moreover, adiponectin ubiquitination was increased in visceral fat of obese pregnant women as compared to lean pregnant women. We further observed that insulin prevents, whereas ER stress and inflammation promote, adiponectin ubiquitination and degradation in differentiated 3T3-L1 adipocytes. We have identified key molecular pathways regulating adiponectin secretion in pregnancy. This information will help us better understand the mechanisms controlling maternal insulin resistance and fetal growth in pregnancy and may provide a foundation for the development of strategies aimed at improving adiponectin production in pregnant women with obesity or gestational diabetes.


2001 ◽  
Vol 90 (1) ◽  
pp. 99-104 ◽  
Author(s):  
Nicole A. Lynch ◽  
Barbara J. Nicklas ◽  
Dora M. Berman ◽  
Karen E. Dennis ◽  
Andrew P. Goldberg

The accumulation of visceral fat is independently associated with an increased risk for cardiovascular disease. The aim of this study was to determine whether the loss of visceral adipose tissue area (VAT; computed tomography) is related to improvements in maximal O2 uptake (V˙o 2 max) during a weight loss (250–350 kcal/day deficit) and walking (3 days/wk, 30–40 min) intervention. Forty obese [body fat 47 ± 1 (SE) %], sedentary (V˙o 2 max 19 ± 1 ml · kg−1 · min−1) postmenopausal women (age 62 ± 1 yr) participated in the study. The intervention resulted in significant declines in body weight (−8%), total fat mass (dual-energy X-ray absorptiometry; −17%), VAT (−17%), and subcutaneous adipose tissue area (−17%) with no change in lean body mass (all P < 0.001). Women with an average 10% increase in V˙o 2 max reduced VAT by an average of 20%, whereas those who did not increaseV˙o 2 max decreased VAT by only 10%, despite comparable reductions in body fat, fat mass, and subcutaneous adipose tissue area. The decrease in VAT was independently related to the change in V˙o 2 max( r 2 = 0.22; P < 0.01) and fat mass ( r 2 = 0.08; P = 0.05). These data indicate that greater improvements inV˙o 2 max with weight loss and walking are associated with greater reductions in visceral adiposity in obese postmenopausal women.


Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 6145-6156 ◽  
Author(s):  
Mary M. N. Nguyen ◽  
Kellie L. K. Tamashiro ◽  
Susan J. Melhorn ◽  
Li Y. Ma ◽  
Stacy R. Gardner ◽  
...  

The visible burrow system (VBS) is a model used to study chronic social stress in colony-housed rats. A hierarchy develops among the males resulting in dominant (DOM) and subordinate (SUB) animals. Hierarchy-associated changes in body weight, body composition, behavior, and neuroendocrine measures have been observed. After 14 d of VBS housing, SUB animals have decreased body weight, elevated corticosterone, and decreased testosterone (T), compared with DOM animals and controls, placing SUB animals in an ideal endocrine state to regain lost body weight as adipose tissue. It is hypothesized that maintaining constant androgen concentrations in SUB males during stress will prevent body weight loss by maintaining more lean body mass. To test this, animals were gonadectomized and implanted with SILASTIC implants containing T, 5α-dihydrotestosterone (DHT), or cholesterol. Implants maintained constant physiological levels of T. Standard intact, T, and DHT implant colonies formed hierarchies, whereas cholesterol colonies did not. Androgen manipulations significantly altered offensive and defensive behaviors only on the first day of VBS housing. After VBS stress, intact, T, and DHT SUB animals weighed less and lost more adipose and lean tissue than DOM and control males, whereas DOM animals primarily lost adipose tissue. However, on recovery, DHT SUB animals maintained more lean tissue than intact SUB animals. Oral glucose tolerance tests revealed that glucose clears faster in stressed T-implanted males that have increased adipose tissue. Overall, these data suggest that constant androgen concentrations in SUB animals do not prevent weight loss and changes in body composition during stress but do so during recovery.


Antioxidants ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 594 ◽  
Author(s):  
Daniela Pellegrino ◽  
Daniele La Russa ◽  
Alessandro Marrone

Chronic kidney disease (CKD) is a major public health problem worldwide and affects both elderly and young subjects. Its main consequences include the loss of renal function, leading to end-stage renal disease, an increased risk of cardiovascular disease, a significant increase in morbidity and mortality, and a decrease in health-related quality of life. This review arose in significant part from work in the authors’ laboratory, complemented by literature data, and was based on a translational approach: we studied the role of many CKD risk factors, such as hypertension, obesity, and oxidative stress/inflammation. The aim was to identify new molecular mechanisms of kidney damage to prevent it through successful behavior modifications. For this purpose, in our studies, both human and animal models were used. In the animal models, we analyzed the mechanisms of renal damage induced by hypertension (spontaneously hypertensive rats) and obesity (cafeteria diet-fed rats), showing that redox disequilibrium in plasma and tissue is extremely important in renal alteration in terms of both oxidative damage (lipid peroxidation, altered expression antioxidant enzymes) and apoptotic pathway (intrinsic/extrinsic) activation. In hemodialysis patients, we explored the correlation between the global oxidative balance and both inflammatory markers and cardiovascular risk, showing a strong correlation between the oxidative index and the blood levels of C-reactive protein and previous cardiovascular events. This multilevel approach allowed us to individually and synergistically analyze some aspects of the complex pathogenic mechanisms of CKD in order to clarify the role of the new amplified risk factors for CKD and to prepare an effective personalized prevention plan by acting on both modifiable and nonmodifiable risk factors.


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