scholarly journals Short-Term Regulation of Adiponectin Secretion in Rat Adipocytes

2011 ◽  
pp. 521-530 ◽  
Author(s):  
T. SZKUDELSKI ◽  
L. NOGOWSKI ◽  
K. SZKUDELSKA
Keyword(s):  
Electron Transport ◽  
Metabolic Diseases ◽  
Biologically Active ◽  
Dibutyryl Camp ◽  
Short Term ◽  
Rat Adipocytes ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Active Substances ◽  
Isolated Rat

Adiponectin belongs to the group of biologically active substances secreted by adipocytes and referred to as adipokines. Disturbances in its secretion and/or action are thought to be involved in the pathogenesis of some metabolic diseases. However, regulation of adiponectin secretion is poorly elucidated. In the present study, short-term regulation of adiponectin secretion in primary rat adipocytes was investigated. Isolated rat adipocytes were incubated in Krebs-Ringer buffer containing 5 mM glucose and insulin alone or in the combination with epinephrine, dibutyryl-cAMP, adenosine A1 receptor antagonist (DPCPX), palmitate, 2-bromopalmitate or inhibitor of mitochondrial electron transport (rotenone). Adipocyte exposure for 2 h to insulin (1-100 nM) significantly increased secretion of adiponectin compared with secretion observed without insulin. Furthermore, secretion of adiponectin from adipocytes incubated with glucose and insulin was reduced by 1 and 2 μM epinephrine, but not by 0.25 and 0.5 μM epinephrine. Under similar conditions, 1 and 2 mM dibutyryl-cAMP substantially diminished secretion of adiponectin, whereas 0.5 mM dibutyryl-cAMP was ineffective. Secretion of adiponectin was found to be effectively decreased by DPCPX. Moreover, adipocyte exposure to rotenone also resulted in a substantial diminution of secretory response of adipocytes incubated for 2 h with glucose and insulin. It was also demonstrated that palmitate and 2-bromopalmitate (0.06-0.5 mM) failed to affect secretion of leptin. The obtained results indicated that in short-term regulation of adiponectin secretion, insulin and epinephrine exert the opposite effects. These effects appeared as early as after 2 h of exposure. Moreover, deprivation of energy or blockade of adenosine action substantially decreased secretion of adiponectin.

scholarly journals Bisphenol A disturbs metabolism of primary rat adipocytes without affecting adipokine secretion

2021 ◽  
Author(s):  
Katarzyna Szkudelska ◽  
Monika Okulicz ◽  
Tomasz Szkudelski
Keyword(s):  
Bisphenol A ◽  
Glucose Oxidation ◽  
Low Doses ◽  
Dibutyryl Camp ◽  
Short Term ◽  
Rat Adipocytes ◽  
Short Term Exposure ◽  
Kinase A ◽  
Isolated Rat ◽  
Direct Activator

AbstractBisphenol A (BPA) is an ubiquitous synthetic chemical exerting numerous adverse effects. Results of rodent studies show that BPA negatively affects adipose tissue. However, the short-term influence of this compound addressing adipocyte metabolism and adipokine secretion is unknown. In the present study, isolated rat adipocytes were exposed for 2 h to 1 and 10 nM BPA. Insulin-induced glucose conversion to lipids along with glucose transport was significantly increased in the presence of BPA. However, basal glucose conversion to lipids, glucose oxidation, and formation of lipids from acetate were unchanged in adipocytes incubated with BPA. It was also shown that BPA significantly increases lipolytic response of adipocytes to epinephrine. However, lipolysis stimulated by dibutyryl-cAMP (a direct activator of protein kinase A) and the antilipolytic action of insulin were not affected by BPA. Moreover, BPA did not influence leptin and adiponectin secretion from adipocytes. Our new results show that BPA is capable of disturbing processes related to lipid accumulation in isolated rat adipocytes. This is associated with the potentiation of insulin and epinephrine action. The effects of BPA appear already after short-term exposure to low doses of this compound. However, BPA fails to change adipokine secretion.

scholarly journals Acipimox stimulates leptin production from isolated rat adipocytes

2002 ◽  
Vol 174 (2) ◽  
pp. 267-272 ◽  
Author(s):  
YL Wang-Fisher ◽  
J Han ◽  
W Guo
Keyword(s):  
Fatty Acids ◽  
Insulin Sensitivity ◽  
Side Effects ◽  
Nicotinic Acid ◽  
Free Fatty Acids ◽  
Dibutyryl Camp ◽  
Similar Extent ◽  
Rat Adipocytes ◽  
Impaired Insulin ◽  
Isolated Rat

Acipimox is a nicotinic acid-derived antilipolytic drug devoid of major side effects, and has been used in a number of human trials. This work reports the effects of Acipimox on leptin production from isolated rat adipocytes, in comparison with nicotinic acid and insulin. For cells isolated from normal animals, all these three reagents stimulated leptin release to a similar extent. Acipimox and nicotinic acid were more potent than insulin in stimulating leptin release from cells isolated from diabetic animals, probably because of impaired insulin sensitivity in cells from these diseased animals. Co-incubation of Acipimox with norepinephrine or dibutyryl cAMP diminished its stimulatory effects on leptin release, in parallel with increased lipolysis, suggesting that intracellular free fatty acids play an important role in mediating leptin production in adipocytes.

scholarly journals Effects of adenosine A1 receptor antagonism on lipogenesis and lipolysis in isolated rat adipocytes

2009 ◽  
pp. 863-871
Author(s):  
T Szkudelski ◽  
K Szkudelska ◽  
L Nogowski
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Synergistic Action ◽  
Adenosine A1 Receptor ◽  
Weak Effect ◽  
Rat Adipocytes ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Release Of Glycerol ◽  
Kinase A

Adenosine is secreted from adipocytes, binds to adenosine A1 receptor and modulates various functions of these cells. In the present study, the effects of an adenosine A1 receptor antagonist (DPCPX; 0.01, 0.1 and 1 μM) on lipogenesis, glucose transport, lipolysis and the antilipolytic action of insulin were tested in rat adipocytes. DPCPX had a very weak effect on lipogenesis and did not significantly affect glucose uptake. In adipocytes incubated with 1 μM DPCPX, lipolysis increased. This effect was blunted by insulin and by a direct inhibitor of protein kinase A. Moreover, 0.1 μM DPCPX substantially enhanced the lipolytic response to epinephrine and increased cAMP in adipocytes. However, DPCPX was ineffective when lipolysis was stimulated by direct activation of protein kinase A. Adipocyte exposure to epinephrine and insulin with or without 0.1 μM DPCPX demonstrated that this antagonist increased the release of glycerol. However, despite the presence of DPCPX, insulin was able to reduce lipolysis. It is concluded that DPCPX had a weak effect on lipogenesis, whereas lipolysis was significantly affected. The partial antagonism of adenosine A1 receptor increased lipolysis in cells incubated with epinephrine alone and epinephrine with insulin due to the synergistic action of 0.1 μM DPCPX and epinephrine.

Long residence time adenosine A1 receptor agonists produce sustained wash-resistant antilipolytic effect in rat adipocytes

2019 ◽  
Vol 164 ◽  
pp. 45-52 ◽  
Author(s):  
Yi Yun ◽  
Jianmin Chen ◽  
Rongfang Liu ◽  
Wenbing Chen ◽  
Chunji Liu ◽  
...  
Keyword(s):  
Residence Time ◽  
Adenosine A1 Receptor ◽  
Receptor Agonists ◽  
Rat Adipocytes ◽  
Adenosine A1 ◽  
A1 Receptor

Inhibition of NMDA receptor-mediated currents in isolated rat hippocampal neurones by adenosine A1 receptor activation

Neuroreport ◽  
1995 ◽  
Vol 6 (8) ◽  
pp. 1097???1100
Author(s):  
Alexandre de Mendon??a ◽  
Ana M. Sebasti??o ◽  
J. Alexandre Ribeiro
Keyword(s):  
Nmda Receptor ◽  
Receptor Activation ◽  
Adenosine A1 Receptor ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Isolated Rat

Abstract P300: A Novel Highly Selective Adenosine A 1 Receptor Agonist (VCP28) Reduces Ischemia/Reperfusion Injury at Concentrations that Do Not Affect Heart Rate

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Paul J White ◽  
Vijay Urmaliya ◽  
Colin W Pouton ◽  
Shane Devine ◽  
Peter Scammells
Keyword(s):  
Heart Rate ◽  
Receptor Agonist ◽  
Left Ventricular ◽  
Adenosine A1 Receptor ◽  
Rat Hearts ◽  
Adenosine A1 ◽  
Si Model ◽  
A1 Receptor ◽  
Cardioprotective Effects ◽  
Isolated Rat

Whilst adenosine A1 receptor agonists have repeatedly been shown to protect the ischaemic myocardium, the clinical use of these agents is limited by strong cardiodepressant effects. The cardioprotective effects of a novel adenosine A1 receptor agonist N6-(2,2,5,5-tetramethylpyrrolidin-1-yloxyl-3-ylmethyl) adenosine (VCP28) were compared with the selective adenosine A1receptor agonist N6-cyclopentyladenosine (CPA) in a H9c2(2–1) cardiac cell line-simulated ischemia (SI) model (12 hours) and a global ischemia (30 minutes) and reperfusion (60 minutes) model in isolated rat heart model. H9c2(2–1) cells were treated with CPA and VCP28 at the start of ischemia for entire ischemic duration, whereas isolated rat hearts were treated at the onset of reperfusion for 15 minutes. In a H9c2(2–1) cell SI model, CPA and VCP28 (100 nM) significantly (P , 0.05, n = 5–6) reduced the proportion of nonviable cells (30.88% 6 2.49% and 16.17% 6 3.77% of SI group, respectively) and lactate dehydrogenase efflux. In isolated rat hearts, CPA and VCP28 significantly (n = 6–8, P , 0.05) improved postischemic contractility (dP/dtmax, 81.69% 6 10.96%, 91.07% 6 19.87% of baseline, respectively), left ventricular developed pressure, and end diastolic pressure and reduced infarct size. The adenosine A1 receptor antagonist DPCPX abolished the cardioprotective effects of CPA and VCP28 in both models. At the concentrations used in the ischaemia models, VCP28 had no effect on heart rate, unlike CPA. In conclusion, the adenosine A1 receptor agonist VCP28 has cardioprotective equal effects to the prototype A1 agonist CPA at concentrations that have no effect on heart rate.

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