scholarly journals Chromium acetate stimulates adipogenesis through regulation of gene expression and phosphorylation of adenosine monophosphate-activated protein kinase in bovine intramuscular or subcutaneous adipocytes

2020 ◽  
Vol 33 (4) ◽  
pp. 651-661 ◽  
Author(s):  
Jongkyoo Kim ◽  
Kiyong Chung ◽  
Bradley J. Johnson

Objective: We hypothesized that Cr source can alter adipogenic-related transcriptional regulations and cell signaling. Therefore, the objective of the study was to evaluate the biological effects of chromium acetate (CrAc) on bovine intramuscular (IM) and subcutaneous (SC) adipose cells.Methods: Bovine preadipocytes isolated from two different adipose tissue depots; IM and SC were used to evaluate the effect of CrAc treatment during differentiation on adipogenic gene expression. Adipocytes were incubated with various doses of CrAc: 0 (differentiation media only, control), 0.1, 1, and 10 μM. Cells were harvested and then analyzed by real-time quantitative polymerase chain reaction in order to measure the quantity of adenosine monophosphate-activated protein kinase-α (<i>AMPK-α</i>), CCAAT enhancer binding protein-β (<i>C/EBPβ</i>), G protein-coupled receptor 41 (<i>GPR41</i>), <i>GPR43</i>, peroxisome proliferator-activated receptor-γ (<i>PPARγ</i>), and stearoyl CoA desaturase (<i>SCD</i>) mRNA relative to ribosomal protein subunit 9 (<i>RPS9</i>). The ratio of phosphorylated-AMPK (pAMPK) to AMPK was determined using a western blot technique in order to determine changing concentration.Results: The high dose (10 μM) of CrAc increased <i>C/EBPβ</i>, in both IM (p = 0.02) and SC (p = 0.02). Expression of <i>PPARγ</i> was upregulated by 10 μM of CrAc in IM but not in SC. Expression of <i>SCD</i> was also increased in both IM and SC with 10 μM of CrAc treatment. Addition of CrAc did not alter gene expression of glucose transporter 4, <i>GPR41</i>, or <i>GPR43</i> in both IM and SC adipocytes. Addition of CrAc, resulted in a decreased pAMPKα to AMPKα ration (p<0.01) in IM.Conclusion: These data may indicate that Cr source may influence lipid filling in IM adipocytes via inhibitory action of AMPK phosphorylation and upregulating expression of adipogenic genes.

Animals ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 1138
Author(s):  
Jingfei Zhang ◽  
Wen Xu ◽  
Hongli Han ◽  
Lili Zhang ◽  
Tian Wang

This study aimed to investigate the effects of leucine with different levels on the insulin resistance in intrauterine growth restriction/retardation (IUGR) piglets. Thirty-two weaned piglets were arranged in a 2 × 2 factorial design and four treatments (n = 8) were as follow: (1) normal weaned piglets fed a basal diet (CONT), (2) IUGR weaned piglets fed a basal diet (IUGR), (3) normal weaned piglets fed a basal diet with the addition of 0.35% l-leucine (C-LEU), and (4) IUGR fed a basal diet with the addition of 0.35% l-leucine (I-LEU) for a 21-days trial. The results showed that compared to the IUGR group, the I-LEU group had higher final body weight and body weight gain, higher serum glucose concentrations, and higher serum insulin concentrations (p < 0.05). The gene expression of phosphatidylinositol 3-kinase p110 gamma, protein kinase adenosine monophosphate-activated γ 3-subunit, glycogen synthase kinase-3 alpha, and glucose transporter type 2 were increased in the I-LEU group as compared to the IUGR group (p < 0.05). It was concluded that dietary leucine supplementation restored serum glucose concentrations, increased insulin and creatinine concentrations, and enhanced protein kinase adenosine monophosphate-activated γ 3-subunit and glucose transporter type 2 expression, suggesting that leucine might play a positive role in hepatic lipid metabolism and glucose metabolism in IUGR.


1996 ◽  
Vol 271 (2) ◽  
pp. E253-E260 ◽  
Author(s):  
C. E. Torgan ◽  
W. E. Kraus

Skeletal muscle exhibits a wide range in functional phenotype in response to changes in physiological demands. We have observed that, in response to changes in work patterns, alterations in gene expression of some proteins coincide with changes in adenylyl cyclase (AC) activity [Kraus, W.E., J.P. Longabaugh, and S. B. Liggett. Am. J. Physiol 263 (Endocrinol. Metab. 26): E266-E230, 1992]. We now examine AC isoform transcript prevalence in various rabbit skeletal muscles and in response to changing work demands. Using reverse transcriptase-polymerase chain reaction, we detected type II AC isoform transcripts in rabbit skeletal muscle. Ribonuclease protection analyses revealed that expression of the type II isoform significantly correlated with the percentage of fast-twitch type IIb/IId fibers (r2 = 0.765, P < 0.01). When a fast-twitch muscle was converted to a slow-twitch muscle via chronic electrical pacing, expression of type II AC mRNA significantly decreased. This response occurred 3 days after the onset of stimulation (78% decrease) and was still present after 21 days of stimulation (76% decrease). As type II AC is relatively insensitive to calcium regulation while sensitive to protein kinase C (PKC) signaling, these data provide further impetus for investigations of protein kinase A and PKC cross-talk signaling mechanisms in the regulation of gene expression.


2018 ◽  
Vol 22 (6) ◽  
pp. 620-626 ◽  
Author(s):  
Garrett N. Cyprus ◽  
Jefferson W. Overlin ◽  
Rafael A. Vega ◽  
Ann M. Ritter ◽  
René Olivares-Navarrete

OBJECTIVECranial suture patterning and development are highly regulated processes that are not entirely understood. While studies have investigated the differential gene expression for different sutures, little is known about gene expression changes during suture fusion. The aim of this study was to examine gene expression in patent, fusing, and fused regions along sagittal suture specimens in nonsyndromic craniosynostosis patients.METHODSSagittal sutures were collected from 7 patients (average age 4.5 months) who underwent minimally invasive craniotomies at the Children’s Hospital of Richmond at VCU under IRB approval. The sutures were analyzed using micro-CT to evaluate patency. The areas were classified as open, fusing, or fused and were harvested, and mRNA was isolated. Gene expression for bone-related proteins, osteogenic and angiogenic factors, transforming growth factor–β (TGF-β) superfamily, and Wnt signaling was analyzed using quantitative polymerase chain reaction and compared with normal sutures collected from fetal demise tissue (control).RESULTSMicro-CT demonstrated that there are variable areas of closure along the length of the sagittal suture. When comparing control samples to surgical samples, there was a significant difference in genes for Wnt signaling, TGF-β, angiogenic and osteogenic factors, bone remodeling, and nuclear rigidity in mRNA isolated from the fusing and fused areas of the sagittal suture compared with patent areas (p < 0.05).CONCLUSIONSIn nonsyndromic sagittal craniosynostosis, the affected suture has variable areas of being open, fusing, and fused. These specific areas have different mRNA expression. The results suggest that BMP-2, FGFR3, and several other signaling pathways play a significant role in the regulation of suture fusion as well as in the maintenance of patency in the normal suture.


2020 ◽  
Vol 38 (1) ◽  
pp. 397-419
Author(s):  
Michael J. Shapiro ◽  
Virginia Smith Shapiro

T cell development involves stepwise progression through defined stages that give rise to multiple T cell subtypes, and this is accompanied by the establishment of stage-specific gene expression. Changes in chromatin accessibility and chromatin modifications accompany changes in gene expression during T cell development. Chromatin-modifying enzymes that add or reverse covalent modifications to DNA and histones have a critical role in the dynamic regulation of gene expression throughout T cell development. As each chromatin-modifying enzyme has multiple family members that are typically all coexpressed during T cell development, their function is sometimes revealed only when two related enzymes are concurrently deleted. This work has also revealed that the biological effects of these enzymes often involve regulation of a limited set of targets. The growing diversity in the types and sites of modification, as well as the potential for a single enzyme to catalyze multiple modifications, is also highlighted.


Genes ◽  
2020 ◽  
Vol 11 (6) ◽  
pp. 641 ◽  
Author(s):  
R. Nicholas Laribee ◽  
Ronit Weisman

The target of rapamycin (TOR) protein kinase is at the core of growth factor- and nutrient-dependent signaling pathways that are well-known for their regulation of metabolism, growth, and proliferation. However, TOR is also involved in the regulation of gene expression, genomic and epigenomic stability. TOR affects nuclear functions indirectly through its activity in the cytoplasm, but also directly through active nuclear TOR pools. The mechanisms by which TOR regulates its nuclear functions are less well-understood compared with its cytoplasmic activities. TOR is an important pharmacological target for several diseases, including cancer, metabolic and neurological disorders. Thus, studies of the nuclear functions of TOR are important for our understanding of basic biological processes, as well as for clinical implications.


2001 ◽  
Vol 357 (3) ◽  
pp. 867-873 ◽  
Author(s):  
Dieter SCHMOLL ◽  
Rolf GREMPLER ◽  
Andreas BARTHEL ◽  
Hans-Georg JOOST ◽  
Reinhard WALTHER

Glucose-6-phosphatase (G6Pase) plays a central role in blood glucose homoeostasis, and insulin suppresses G6Pase gene expression by the activation of phosphoinositide 3-kinase (PI 3-kinase). Here, we show that the phorbol ester PMA decreases both basal and dexamethasone/cAMP-induced expression of a luciferase gene under the control of the G6Pase promoter in transiently transfected H4IIE hepatoma cells. This regulation was suppressed by the inhibitors of the mitogen-activated protein kinase/extracellular-signal-regulated kinase kinase (MEK), PD98059 and U0126, but not by the inhibitor of PI 3-kinase, LY294002. The co-expression of a constitutively active mutant of MEK mimicked the regulation of G6Pase promoter activity by PMA. The effect of PMA on both basal and induced G6Pase gene transcription was impaired by the overexpression of a dominant negative MEK construct, as well as by the expression of mitogen-activated protein kinase phosphatase-1. The mutation of the forkhead-binding sites within the insulin-response unit of the G6Pase promoter, which decreases the effect of insulin on G6Pase gene expression, did not alter the regulation of gene expression by PMA. The data show that PMA decreases G6Pase gene expression by the activation of MEK and extracellular-signal regulated protein kinase. With that, PMA mimics the effect of insulin on G6Pase gene expression by a different signalling pathway.


1987 ◽  
Vol 7 (8) ◽  
pp. 3004-3007
Author(s):  
M W White ◽  
A K Oberhauser ◽  
C A Kuepfer ◽  
D R Morris

Two categories of mitogen-induced mRNAs were defined in T lymphocytes. The type 1 messages (represented by c-myc) were regulated transcriptionally, and their expression seemed to be calmodulin dependent. The type 2 messages (ornithine decarboxylase, actin, and alpha-tubulin) were regulated posttranscriptionally through activation of protein kinase C.


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