scholarly journals A protein kinase inhibitor in brown adipose tissue of developing rats

1974 ◽  
Vol 138 (2) ◽  
pp. 195-199 ◽  
Author(s):  
Josef P. Skala ◽  
George I. Drummond ◽  
Peter Hahn
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
Cyclic Amp ◽  
Brown Adipose Tissue ◽  
Inhibitory Activity ◽  
Kinase Inhibitor ◽  
Protein Kinase Inhibitor ◽  
Supernatant Fraction ◽  
Brown Adipose ◽  
Tissue Homogenates

A heat-stable protein was extracted from brown adipose tissue of infant rats that inhibited both purified bovine heart protein kinase and a crude preparation of protein kinase from brown fat. It did not act as an adenosine triphosphatase nor did it exert its effect by proteolytic action. Inhibition of protein kinase was affected in both the presence and the absence of cyclic AMP. Most of the inhibitory activity was present in the 100000g supernatant fraction of tissue homogenates. Inhibitory activity was highest perinatally and it declined 10 days after birth. It is suggested that the protein kinase inhibitor may play a role in regulating cyclic AMP actions.

Protein kinases in brown adipose tissue of developing rats: substrate specificities, separation, and changes in activity during development

1978 ◽  
Vol 56 (9) ◽  
pp. 869-874 ◽  
Author(s):  
Josef P. Skala ◽  
Brian L. Knight
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
Brown Adipose Tissue ◽  
Kinase Activity ◽  
Specific Activity ◽  
Brown Fat ◽  
Supernatant Fraction ◽  
Protein Kinase Activity ◽  
Nonhistone Proteins ◽  
Brown Adipose

Protein kinase activity in the 100 000 × g supernatant fraction of brown adipose tissue was assayed with various proteins as substrates. Greatest activity was obtained with histone subfraction f2b and the lowest activity with protamine. cAMP stimulated the phosphorylation of histones but not that of the other proteins. The specific activity of protein kinase in brown fat of rats changed during infancy, and the pattern of changes was different with different protein substrates.Electrophoresis of the tissue-soluble extract gave nine major bands of protein kinase activity. These were assayed on the gels under the optimal conditions for each substrate. Five of the bands were histone kinases and gave little activity with nonhistone proteins. Two bands gave their greatest activity with phosvitin or casein. Protamine and arginine-rich histone were particularly good substrates for the two remaining bands. The activity in each band exhibited a different and distinct pattern of ontogenic development, which was not affected by the nature of the protein used for the assay. There was a reasonable similarity between the overall developmental profile for the rate of phosphorylation of each substrate calculated from the sum of activities determined on the individual bands and the profile directly determined in the whole soluble fraction.Both the direct assay and the electrophoretic results indicate that brown fat contains a number of protein kinase activities that can be distinguished by their specificities for protein substrate and by the pattern of changes in their activities during development. There were three main patterns of ontogenic changes in activity: one decreased progressively from high values in late foetuses; the second showed a marked fall in activity during the 3rd week after birth; and in the third, the activity rose after birth and then remained constant. The greatest changes in kinase activity thus occur during the periods when there are pronounced changes in the rates of proliferation and differentiation in brown fat, in its capacity to produce heat, and in the diet of the animal. It seems possible that the different types of protein kinase carry out phosphorylations involved in the regulation of different processes in brown fat.

Control of brown adipose tissue lipolysis and respiration by adenosine

1983 ◽  
Vol 245 (6) ◽  
pp. E555-E559 ◽  
Author(s):  
D. Szillat ◽  
L. J. Bukowiecki
Keyword(s):  
Adipose Tissue ◽  
Cyclic Amp ◽  
Palmitic Acid ◽  
Brown Adipose Tissue ◽  
Brown Adipocyte ◽  
Tissue Respiration ◽  
Dibutyryl Cyclic Amp ◽  
Response Curves ◽  
Brown Adipose ◽  
Stimulation Of

Adenosine competitively inhibited the stimulatory effects of (-)-isoproterenol on lipolysis and respiration in hamster brown adipocytes. The low value of the apparent ki for respiratory inhibition by adenosine (7 nM) indicated that the nucleoside may control brown adipocyte function under physiological concentrations. Significantly, the dose-response curves for isoproterenol stimulation of lipolysis and respiration were both shifted by adenosine to higher agonist concentrations by the same order of magnitude, providing additional evidence for a tight coupling between lipolysis and respiration. The inhibitory effects of adenosine were rapidly reversed by a) adenosine deaminase, b) agents known to increase intracellular cyclic AMP levels (isoproterenol, isobutylmethylxanthine, dibutyryl cyclic AMP), and c) direct stimulation of respiration with palmitic acid. These results, combined with the fact that adenosine failed to affect respiration evoked either by dibutyryl cyclic AMP or by palmitic acid, strongly indicate that adenosine regulates brown adipose tissue respiration at an early metabolic step of the stimulus-thermogenesis sequence, most probably at the level of the adenylate cyclase complex.

scholarly journals Nicotine Improves Obesity and Hepatic Steatosis and ER Stress in Diet-Induced Obese Male Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (5) ◽  
pp. 1679-1689 ◽  
Author(s):  
Patricia Seoane-Collazo ◽  
Pablo B. Martínez de Morentin ◽  
Johan Fernø ◽  
Carlos Diéguez ◽  
Rubén Nogueiras ◽  
...  
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Adipose Tissue ◽  
Energy Balance ◽  
Protein Kinase ◽  
Brown Adipose Tissue ◽  
Male Rats ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Amp Activated Protein Kinase

Nicotine, the main addictive component of tobacco, promotes body weight reduction in humans and rodents. Recent evidence has suggested that nicotine acts in the central nervous system to modulate energy balance. Specifically, nicotine modulates hypothalamic AMP-activated protein kinase to decrease feeding and to increase brown adipose tissue thermogenesis through the sympathetic nervous system, leading to weight loss. Of note, most of this evidence has been obtained in animal models fed with normal diet or low-fat diet (LFD). However, its effectiveness in obese models remains elusive. Because obesity causes resistance towards many factors involved in energy homeostasis, the aim of this study has been to compare the effect of nicotine in a diet-induced obese (DIO) model, namely rats fed a high-fat diet, with rats fed a LFD. Our data show that chronic peripheral nicotine treatment reduced body weight by decreasing food intake and increasing brown adipose tissue thermogenesis in both LFD and DIO rats. This overall negative energy balance was associated to decreased activation of hypothalamic AMP-activated protein kinase in both models. Furthermore, nicotine improved serum lipid profile, decreased insulin serum levels, as well as reduced steatosis, inflammation, and endoplasmic reticulum stress in the liver of DIO rats but not in LFD rats. Overall, this evidence suggests that nicotine diminishes body weight and improves metabolic disorders linked to DIO and might offer a clear-cut strategy to develop new therapeutic approaches against obesity and its metabolic complications.

β-Lapachone Regulates Obesity through Modulating Thermogenesis in Brown Adipose Tissue and Adipocytes: Role of AMPK Signaling Pathway

2019 ◽  
Vol 47 (04) ◽  
pp. 803-822 ◽  
Author(s):  
Hyun Jeong Kwak ◽  
Mi-Young Jeong ◽  
Jae-Young Um ◽  
Jinbong Park
Keyword(s):  
Adipose Tissue ◽  
Protein Kinase ◽  
Brown Adipose Tissue ◽  
Signaling Pathway ◽  
Uncoupling Protein ◽  
Therapeutic Implication ◽  
Mitogen Activated Protein Kinase ◽  
Ampk Signaling ◽  
Compound C ◽  
Brown Adipose

Activation of brown adipose tissue (BAT) has been proposed as a promising target against obesity due to its increased capacity for thermogenesis. In this study, we explored the effect of [Formula: see text]-Lapachone ([Formula: see text]L), a compound obtained from the bark of the lapacho tree, against obesity. In vivo administration of [Formula: see text]L into either high fat diet (HFD)-induced obese C57BL6 mice and genetically obese Lepr[Formula: see text] mice prevented body weight gain, which was associated with tissue weight loss of white adipose tissue (WAT). In addition, [Formula: see text]L elevated thermogenic proteins including uncoupling protein 1 (UCP1) and mitochondrial count in BAT and human adipose tissue-derived mesenchymal stem cells (hAMSCs). [Formula: see text]L also induced AMP-activated protein kinase (AMPK) phosphorylation, subsequent upregulation of acetyl-CoA carboxylase (ACC) and UCP1, and these effects were diminished by AMPK inhibitor compound C, suggesting that AMPK underlies the effects of [Formula: see text]L. Mitogen-activated protein kinase pathways participated in the thermogenesis of [Formula: see text]L, specifically p38, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase 1/2 (ERK1/2) were activated by [Formula: see text]L treatment in hAMSCs. Additionally, inhibitors of p38/JNK/ERK1/2 abrogated the activity of [Formula: see text]L. Taken together, [Formula: see text]L exerts anti-obese effects by inducing thermogenesis mediated by AMPK signaling pathway, suggesting that [Formula: see text]L may have a potential therapeutic implication of obesity. Taken together, [Formula: see text]L exerts anti-obese effects by not only inducing thermogenesis on brown adipocytes but also inducing the browning of white adipocytes. The anti-obese effect of [Formula: see text]L is mediated by AMPK signaling pathway, suggesting that [Formula: see text]L may have potential therapeutic implication of obesity.

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