Adiponectin and Its Receptors in Diabetic Kidney Disease: Molecular Mechanisms and Clinical Potential

Zha, Dongqing; Wu, Xiaoyan; Gao, Ping

doi:10.1210/en.2016-1765

Cited by 78 publications

(61 citation statements)

References 84 publications

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“…Therefore, adiponectin has emerged as an important target against lipotoxicity-mediated harmful effects [226]. Different therapeutic approaches are under development aiming to increase adiponectin serum levels or adiponectin receptor expression/activity [227].…”

Section: Adiponectin Receptor Agonistsmentioning

confidence: 99%

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

Opazo-Ríos

Mas

Marín-Royo

et al. 2020

IJMS

171

132

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Lipotoxicity is characterized by the ectopic accumulation of lipids in organs different from adipose tissue. Lipotoxicity is mainly associated with dysfunctional signaling and insulin resistance response in non-adipose tissue such as myocardium, pancreas, skeletal muscle, liver, and kidney. Serum lipid abnormalities and renal ectopic lipid accumulation have been associated with the development of kidney diseases, in particular diabetic nephropathy. Chronic hyperinsulinemia, often seen in type 2 diabetes, plays a crucial role in blood and liver lipid metabolism abnormalities, thus resulting in increased non-esterified fatty acids (NEFA). Excessive lipid accumulation alters cellular homeostasis and activates lipogenic and glycogenic cell-signaling pathways. Recent evidences indicate that both quantity and quality of lipids are involved in renal damage associated to lipotoxicity by activating inflammation, oxidative stress, mitochondrial dysfunction, and cell-death. The pathological effects of lipotoxicity have been observed in renal cells, thus promoting podocyte injury, tubular damage, mesangial proliferation, endothelial activation, and formation of macrophage-derived foam cells. Therefore, this review examines the recent preclinical and clinical research about the potentially harmful effects of lipids in the kidney, metabolic markers associated with these mechanisms, major signaling pathways affected, the causes of excessive lipid accumulation, and the types of lipids involved, as well as offers a comprehensive update of therapeutic strategies targeting lipotoxicity.

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Section: Adiponectin Receptor Agonistsmentioning

confidence: 99%

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

Opazo-Ríos

Mas

Marín-Royo

et al. 2020

IJMS

171

132

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“…In addition, overexpression of mTOR protein during this condition leads to renal damage. 23 HEK-293 cells under HG conditions showed mTOR and p-mTOR upregulation, compared with the normal glucose conditions. Our results indicated that APN (100 ng/mL) can significantly reduce the expression of mTOR and p-mTOR.…”

Section: Discussionmentioning

confidence: 86%

“…In addition, overexpression of mTOR protein during this condition leads to renal damage 23. Cell viabilities at (A) 24 and (B) 48 hours significantly decreased, under high-glucose condition and APN improved cell viabilities.…”

mentioning

confidence: 99%

Prevention of kidney cell damage in hyperglycaemia condition by adiponectin

Esmaeili

Motamedrad

Hemmati

et al. 2019

Cell Biochemistry & Function

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Adiponectin (APN) is an adipocytokine, secreted from adipose tissue and has antiinflammatory, anti-ageing, and antidiabetic properties. Hyperglycaemia can damage the renal cells, and mammalian target of rapamycin (mTOR), along with Sirtuin 1 (SIRT1), have an important role in kidney cell response to hyperglycaemia. Therefore, understanding the relationship between adiponectin, mTOR, and SIRT1 proteins is beneficial for deciphering the mechanism of adiponectin function. In this study, Human Embryonic Kidney-293 (HEK-293) cells were cultured under normal and high-glucose condition, with and without APN (1, 10, and 100 ng/mL) for 48 hours. mTOR protein expression was evaluated by western blot analysis, and SIRT1 protein was assessed using ELISA method. To evaluate hyperglycaemia-mediated cytotoxicity, cell viability was determined using MTT assay. Data showed that APN in high dose (100 ng/mL) significantly reduced the expression of mTOR and p-mTOR, increased SIRT1 protein, and also improved cell viability compared with the control high glucose (p ≤ 0.05). According to this results, APN can be useful in preventing renal cell damage, by affecting on the expression of mTOR and SIRT1 proteins, as well as increasing the survival of kidney cells in hyperglycaemia conditions. Significance of the study: Adiponectin triggered mTOR/p-mTOR/SIRT1 pathway and decreased cell death in human kidney cells. Our findings provide preliminary experimental data that support further studies on the potential therapeutic role of adiponectin in diabetes and diabetic-induced metabolic complications.

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“…Адипонектин является противовоспалительным адипокином и сенсибилизатором инсулина [15]. Защита адипонектином сосудов может быть связана с улучшением эндотелиальной дисфункции, снижением окислительного стресса и усилением экспрессии синтазы эндотелиального оксида азота за счет активации аденозиновой 5'-монофосфат-активированной протеинкиназы с помощью AdipoR1 и дей ствия рецептора, активированного пролифератором пероксисом (PPAR) -α сигнальным путем AdipoR2 [15].…”

Section: Discussionunclassified

The state of the main arteries, vascular age in patients with arterial hypertension and obesity: the role of leptin and adiponectin

Стаценко

Деревянченко

2019

Russ J Cardiol

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Aim.To study the state of the main arteries and vascular age in conjunction with the level of leptin and adiponectin in patients with arterial hypertension (AH) and obesity.Material and methods. One hundred and twenty patients with AH stage II aged from 45 to 65 years were divided into 3 groups depending on body mass index (BMI). Group 1 was represented by patients with AH and normal BMI, the 2 group was represented by patients with AH and excessive BMI, the 3 group was represented by patients with AH in combination with obesity. A standard clinical examination was performed, the stiffness of the vascular wall was measured by measuring the pulse wave velocity (PWV) of the muscle and elastic vessels (PWVe), vascular age was calculated, and the laboratory markers of obesity were determined.Results.High percentage of visceral obesity was observed: 20,0% among people with normal BMI, 64,4% among overweight people and 100% among people with obesity (differences between 1 and 2, 1 and 3, 2 and 3 groups are reliable). A statistically significant increase in PWVe was detected in patients with AH and obesity in comparison with patients with AH and normal body weight (9,8 [8,5; 11,3] vs 8,0 [79; 8,1] m/s). Vascular age was higher in patients with AH and overweight or obesity compared with patients with AH and normal weight (670 [60,0; 76,0], 68,0 [60,0; 72,0] vs 58,0 [57,0; 60,0] years, respectively). A statistically significant increase in the concentration of leptin (6,9 [4,5; 15,1] vs 19,0 [74; 42,7] vs 53,8 [38,4; 75,8] ng/ml) was detected, as well as a decrease in adiponectin concentration from the 1 to the 3 group (44,9 [36,6; 55,8] vs 16,5 [12,5; 24,7] vs 18,6 [15,3; 22,4] ng/ml, respectively).Correlation analysis revealed the presence of highly reliable relationships between the parameters of rigidity of the main arteries and laboratory markers of obesity.Conclusion.The results indicated a negative effect of hyperleptinemia and hypoadiponectinemia on the elasticity of the vascular wall of the main arteries and the vascular age in hypertensive patients with its combination with overweight or obesity.

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Adiponectin and Its Receptors in Diabetic Kidney Disease: Molecular Mechanisms and Clinical Potential

Cited by 78 publications

References 84 publications

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

Lipotoxicity and Diabetic Nephropathy: Novel Mechanistic Insights and Therapeutic Opportunities

Prevention of kidney cell damage in hyperglycaemia condition by adiponectin

The state of the main arteries, vascular age in patients with arterial hypertension and obesity: the role of leptin and adiponectin

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