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PubMed1999

Rapid screening of specific changes in mRNA in thyroid carcinomas by sequence specific-differential display: decreased expression of acid ceramidase mRNA in malignant and benign thyroid tumors.

Sequence specific-differential display (SS-DD) is a powerful method for screening significant changes in gene expression between normal and malignant tissues. Using this method, we detected 3 genes for which the expression is much decreased in thyroid tumors. After sub-cloning and sequencing analysis, one of the genes was revealed to be acid ceramidase (AC). The expression of AC in normal thyroids and thyroid tumors was examined by semi-quantitative reverse-transcription-polymerase-chain-reaction (RT-PCR). Obvious decreases in the expression of AC mRNA were observed in 5/6 follicular adenomas, 2/2 adenomatous goiters, 3/6 papillary carcinomas and 1/2 follicular carcinomas. To confirm this result, real-time quantitative PCR analysis (TaqMan PCR) was carried out. The relative expression level of AC mRNA compared with that of GAPDH mRNA was reduced in follicular adenomas, follicular carcinomas, and papillary carcinomas. Further, the expression of AC mRNA was extremely reduced in 2 anaplastic carcinomas. These results suggest a possible relationship between thyroid tumorigenesis and the expression of AC mRNA. Moreover, the increased expression of AC mRNA in normal thyroid tissues suggests some fundamental roles of AC in thyroid function.

Acid Ceramidase↗
PubMed2003

Constitutive expression of p55TNFR mRNA and mitogen-specific up-regulation of TNF alpha and p75TNFR mRNA in mouse brain.

Serum tumor necrosis factor (TNF) functions as a mediator of the immune-to-brain axis. Numerous TNF receptor-mediated effects on the nervous system are described but the knowledge about the regional and cellular expression of TNF receptor p55TNFR and p75TNFR in vivo is far from being complete. It is unclear whether TNF mediates its neuroimmune effects alone or in combination with other factors, e.g., bacterial mitogens. Here, we investigated the distribution of TNFalpha, p55TNFR, and p75TNFR in normal mouse brain and examined the stimulus-specific effects of lipopolysaccharide (LPS) and staphylococcal enterotoxin B (SEB) on the expression of the cerebral TNF system. Both mitogens caused enhanced TNFalpha serum levels and induced c-fos mRNA in the paraventricular nucleus but exhibited different effects on the cerebral gene expression of the TNF system. LPS but not SEB rapidly induced TNFalpha mRNA in circumventricular organs (CVOs) followed by spreading of TNFalpha mRNA into brain parenchyma close to the CVOs. The p55TNFR gene was constitutively expressed in many neurons with high levels in brainstem motor nuclei and in neurons of the sensory mesencephalic trigeminal nucleus. Moderate levels of p75TNFR mRNA were seen in single cells scattered throughout the brain in a pattern resembling microglia. Neither LPS nor SEB modulated the p55TNFR gene expression in any region or cell type of the brain, and LPS but not SEB induced p75TNFR mRNA in the CVOs. Thus, enhanced TNF serum levels able to stimulate c-fos mRNA expression in the paraventricular nucleus did not necessarily result in a modulation of the cerebral TNF system.

Animals↗
PubMed1993

Differential induction of T cell cytokine mRNA in Epstein-Barr virus-transformed B cell clones: constitutive and inducible expression of interleukin-4 mRNA.

Clones of human B lymphocytes, obtained after immortalization with Epstein-Barr virus (EBV) of single CD19+ B cells and expansion in the absence of human T lymphocytes, produced mRNA for the T cell cytokines interleukin(IL)-2, IL-4, and interferon (IFN)-gamma. As detected by reverse transcriptase-polymerase chain reaction, IL-2 mRNA was expressed only after stimulation with the combination of phorbol 12-myristate 13-acetate (PMA) plus ionomycin. IL-4 mRNA was constitutively detectable in all (10/10) EBV-transformed B cell clones, and the mRNA for IFN-gamma was constitutively present in half of the clones. In contrast to IL-2 mRNA, the expression of IL-4 and IFN-gamma mRNA could be increased by PMA alone. Most of the clones produced IL-2 bioactivity and immunoreactive protein, but neither IL-4 nor IFN-gamma protein secretion was detected. The intriguing question raised by these results is whether IL-2 secretion could contribute to the immune control of EBV-infected B lymphocytes by cytolytic T cells, and whether normal B lymphocytes can potentially be induced to express certain cytokines including IL-4 in response to the appropriate activation signals.

B-Lymphocytes↗
PubMed1995

Regulation of interferon-gamma mRNA in a cytolytic T cell clone: Ca(2+)-induced transcription followed by mRNA stabilization through activation of protein kinase C or increase in cAMP.

Activation pathways inducing the expression of the interferon (IFN)-gamma gene in a cytotoxic T lymphocyte (CTL) clone were studied for their effects on transcription and on mRNA stability. IFN-gamma was secreted by the CTL clone in response to the Ca2+ ionophore ionomycin when used in conjunction with either protein kinase C (PKC)-activating phorbol 12-myristate 13-acetate (PMA) or with agents increasing cAMP, including prostaglandin E2. We describe that ionomycin induced IFN-gamma gene transcription, which was totally inhibited in the presence of cyclosporin A (CSA), an immunosuppressant forming a calcineurin-inhibiting complex with cyclophilin. Ionomycin did not, however, permit accumulation of IFN-gamma mRNA. Activation of PKC by PMA or of cAMP-dependent protein kinase through increase in cAMP had no transcription-inducing effect, either alone or in conjunction with ionomycin, as measured in run on assays of the IFN-gamma gene. When transcription of the IFN-gamma gene, initiated in the presence of ionomycin and an agent increasing intracellular cAMP, was inhibited by CSA in the absence of PKC or cAMP-dependent protein kinase activation, the IFN-gamma mRNA was rapidly degraded (half-life = 30 min). When either PKC was activated or intracellular cAMP was increased at the time of inhibition with CSA, a stabilizing effect was observed on IFN-gamma mRNA, which led to an increase in secreted IFN-gamma. These effects were selective, they did not affect the rate of transcription of the actin gene, nor the accumulation of actin mRNA. These results show that (i) post-transcriptional events can be critical for IFN-gamma expression in activated lymphocytes, and (ii) specific stabilization of IFN-gamma mRNA can be mediated by activation of two different protein kinases involved in T cell activation.

Animals↗
PubMed1989

Iron regulation of transferrin receptor mRNA levels requires iron-responsive elements and a rapid turnover determinant in the 3' untranslated region of the mRNA.

Post-transcriptional regulation of transferrin receptor mRNA levels by iron is mediated by a portion of the 3' untranslated region (UTR) of the mRNA. We have previously shown that a 678 nucleotide fragment of the 3'UTR contains the regulatory element(s). Within this region are five RNA structures which resemble the iron-responsive element (IRE) in the 5' untranslated region of the ferritin mRNA which is regulated translationally by iron. The IREs from the ferritin and transferrin receptor mRNAs compete in an in vitro assay for interaction with a cytoplasmic protein; the activity of this IRE-binding protein is dependent upon the iron status of the cells. Based on further deletion analysis reported here, the sequence required for iron regulation of the transferrin receptor have been limited to 250 nucleotides which we have produced synthetically and cloned. This sequence, which contains three IREs, is capable of producing iron-dependent regulation of transferrin receptor levels. Removal of the three IREs from the synthetic element results in loss of iron regulation. Moreover, deletion of a single cytosine residue from each of the three IREs in the synthetic regulatory element eliminates high-affinity binding to the IRE-binding protein in vitro and results in low levels of iron-independent transferrin receptor expression, consistent with production of a constitutively unstable mRNA. These data indicate that the ability of the mRNA to interact with the IRE-binding protein is required for regulation of transferrin receptor mRNA levels by iron.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Alterations of collagen mRNA expression during retinoic acid induced chondrocyte modulation: absence of untranslated alpha 1(I) mRNA in hyaline chondrocytes.

Retinoic acid (RA) has been shown to rapidly modulate the collagen expression pattern of chondrocytes in vitro at doses of 1-10 microM. Embryonic chicken sternal chondrocytes stop synthesizing the cartilage-specific type II collagen within 2-4 days of RA treatment and turn on the synthesis of types I and III collagen and fibronectin. While suppression of type II collagen synthesis and onset of type III collagen and fibronectin synthesis have been shown to be regulated at the transcriptional level, conflicting data are available on a possible post-translational regulation of alpha 1(I) collagen gene expression. In this study we demonstrate by comparing a commonly used alpha 1(I) cDNA probe from the 3' end of the alpha 1(I) mRNA with a newly prepared alpha 1(I) cDNA probe from the 5' end (p1E1) that--in contrast to previous reports--chicken sternal chondrocytes do not contain untranslated alpha 1(I) mRNA which may become translatable after RA treatment. By in situ hybridization we show the absence of cytoplasmic alpha 1(I) mRNA from chondrocytes and its presence in the perichondrium of sternal cartilage. Perichondral cells might have contaminated sternal chondrocyte preparations, explaining low levels of alpha 1(I) mRNA seen by Northern hybridization and RNase protection assays of chicken sternal cartilage mRNA even with the p1E1 probe. We show by Northern hybridization and metabolic labeling with 3H-proline followed by SDS-gel electrophoresis that retinoic acid at 3 microM suppresses type II, IX, and X collagen gene expression within 2 days both at the mRNA and protein level and induces the onset of alpha 1(I), alpha 2(I), and alpha 1(III) expression within 3 days. No expression of CRABP, the cellular retinoic acid binding protein, was seen in RA-treated or control chondrocytes, indicating that CRABP protein is not involved in the RA-induced modulation of the chondrocytes.

Animals↗
PubMed1995

Regulation of heme oxygenase mRNA in mesangial cells: prostaglandin E2 negatively modulates interleukin-1-induced heme oxygenase-1 mRNA.

Heme oxygenase (EC 1.14.99.3) is the rate-limiting enzyme in heme catabolism. Several lines of evidence suggest a possible role for heme oxygenase in the inflammatory process and in cellular signaling. We have evaluated the regulation of heme oxygenase-1 mRNA induction by the inflammatory stimuli, phorbol 12,13-myristate acetate, heat shock and interleukin-1 beta in cultured rat mesangial cells. Phorbol 12,13-myristate acetate and heat shock rapidly (maximal at 2-3 hrs) induced heme oxygenase-1 mRNA. The effect of interleukin-1 beta on heme oxygenase-1 mRNA induction was slower (maximal at 12 hrs) and modest. However, in the presence of a cyclooxygenase inhibitor, indomethacin, interleukin-1 beta strongly induced heme oxygenase-1 mRNA. The addition of exogenous PGE2 reversed the effect of indomethacin. These data suggest that pro-inflammatory stimuli increase heme oxygenase-1 mRNA expression in rat mesangial cells and that interleukin-1 beta-induced heme oxygenase-1 mRNA level is negatively modulated by PGE2.

Animals↗
PubMed1999

The AU-rich 3' untranslated region of human MDR1 mRNA is an inefficient mRNA destabilizer.

The human multidrug resistance gene MDR1 encodes a membrane-bound protein, referred to as P-glycoprotein, that acts as a pump to extrude toxins from cells. The 3' untranslated region (3'UTR) of the human MDR1 mRNA is very AU-rich (70%) and contains AU-rich sequences similar to those shown to confer rapid decay on c-myc, c-fos, and lymphokine mRNAs. We tested the ability of the MDR1 3'UTR to act as an mRNA destabilizing element in the human hepatoma cell line HepG2. The MDR1 mRNA has an intermediate half-life of 8 h in HepG2 cells compared to a half-life of 30 min for c-myc mRNA. The MDR1 mRNA half-life was prolonged to >20 h upon treatment with the protein synthesis inhibitor cycloheximide. We constructed expression vectors containing the human beta-globin coding region with the 3'UTR from either MDR1 or c-myc. The c-myc 3'UTR increased the decay of the chimeric mRNA, but the MDR1 3'UTR had no effect. We tested the ability of MDR1 3'UTR sequences to compete for interaction with AU-binding proteins in cell extracts; MDR1 RNA probes had a fivefold lower affinity for AU-binding proteins that interact with the c-myc AU-rich 3'UTR. Overall, our data suggest that the MDR1 3'UTR does not behave as an active destabilizing element in HepG2 cells.

3' Untranslated Regions↗
PubMed1993

Detection of a novel sepiapterin reductase mRNA: assay of mRNA in various cells and tissues of various species.

Fragments of cDNA coding for rat, murine, and human sepiapterin reductase (SR) were amplified by PCR via primer positioning close to the reported 3'-end of the coding region in the rat enzyme. They were sequenced and used as probes for mRNA detection. Northern blot analysis detected two mRNA species for SR. Their sizes were 1.3 and 2.1 kb for rat, 1.3 and 2.3 kb for mouse, and 1.6 and 2.1 kb for human cell lines. Comparison of rat cell lines and rat tissues indicated that in tissues only the 1.3-kb species is present. Washing of the Northern blots under different stringency conditions indicated a more stable interaction of the 1.3-kb mRNA species with the cDNA probe as compared to the 2.3-kb species. The 1.3-kb species corresponds to the reported 28.2-kDa molecular mass of rat SR monomer. SR mRNA expression is absent in the human NK-like cell line YT and in the murine erythroleukemia subclone B8/3, which both lack SR activity. Moreover, the relative mRNA expression correlates with the enzymatic activities of different cell lines within the same species. This indicates that SR activity is regulated by its steady state mRNA levels.

Alcohol Oxidoreductases↗
PubMed2002

Short-term infusion of LongR(3) insulin-like growth factor (IGF)-I decreases hepatic IGF-I mRNA but not IGF binding protein-3 mRNA expression in pigs.

Infusion of pigs with an insulin-like growth factor-I (IGF-I) analogue (LongR(3)IGF-I) that does not bind to IGF-binding proteins decreases growth rate and the plasma concentration of growth hormone (GH), IGF-I, IGFBP-3, and insulin. This study was designed to determine whether the decrease is due to changes in IGF-I and IGFBP-3 gene expression. IGF-I or LongR(3)IGF-I (180 microg/kg/day) was infused into 55-kg finisher pigs for 4 days using Travenol infuser pumps. Plasma IGF-I concentration was measured by radioimmunoassay and plasma IGFBP-3 and IGFBP-2 were estimated by Western ligand blotting. Steady-state levels of IGF-I and IGFBP-3 mRNA were measured by RNase protection assay. Neither IGF-I nor LongR(3)IGF-I had a significant effect on hepatic IGF-I class 1 mRNA expression, whereas hepatic IGF-I class 2 mRNA expression was significantly reduced by both peptides. Plasma IGFBP-3 levels were unaffected by IGF-I treatment but were reduced by LongR(3)IGF-I treatment. The decrease in IGFBP-3 was not due to decreased gene expression in porcine liver or kidney, since neither IGF-I nor LongR(3)IGF-I treatment altered IGFBP-3 mRNA. This study infers a direct effect of the IGF analogue LongR(3)IGF-I on GH through its inhibition of plasma IGF-I concentration and class 2 IGF-I mRNA. The decrease in plasma IGFBP-3 was not accompanied by a decrease in hepatic or renal IGFBP-3 mRNA, suggesting that in this case, plasma IGFBP-3 protein levels are posttranslationally regulated or are derived from tissues other than liver or kidney.

Animals↗
PubMed1999

E. coli RpsO mRNA decay: RNase E processing at the beginning of the coding sequence stimulates poly(A)-dependent degradation of the mRNA.

The rpsO mRNA of E. coli encoding ribosomal protein S15 is destabilized by poly(A) tails posttranscriptionally added by poly(A)polymerase I. We demonstrate here that polyadenylation also contributes to the rapid degradation of mRNA fragments generated by RNase E. It was already known that an RNase E cleavage occurring at the M2 site, ten nucleotides downstream of the coding sequence of rpsO, removes the 3' hairpin which protects the primary transcript from the attack of polynucleotide phosphorylase and RNase II. A second RNase E processing site, referred to as M3, is now identified at the beginning of the coding sequence of rpsO which contributes together with exonucleases to the degradation of messengers processed at M2. Cleavages at M2 and M3 give rise to mRNA fragments which are very rapidly degraded in wild-type cells. Poly(A)polymerase I contributes differently to the instability of these fragments. The M3-M2 internal fragment, generated by cleavages at M3 and M2, is much more sensitive to poly(A)-dependent degradation than the P1-M2 mRNA, which exhibits the same 3' end as M3-M2 but harbours the 5' end of the primary transcript. We conclude that 5' extremities modulate the poly(A)-dependent degradation of mRNA fragments and that the 5' cleavage by RNase E at M3 activates the chemical degradation of the rpsO mRNA.

Base Sequence↗
PubMed1994

Kappa 1 receptor mRNA distribution in the rat CNS: comparison to kappa receptor binding and prodynorphin mRNA.

Three opioid receptor types have been identified in the CNS and periphery that are referred to as mu, delta, and kappa. The present study examines the mRNA distribution of the kappa 1 receptor in the rat brain and compares it to the distribution of kappa receptor-binding sites and prodynorphin mRNA using a combination of in situ hybridization and receptor autoradiographic techniques. kappa 1 receptor mRNA was localized with a cRNA probe generated with a BamHI-HindIII cDNA fragment of the rat kappa 1 receptor and corresponds to the last 45 bp of the protein coding region and 728 nucleotides of the 3' untranslated region. Prodynorphin mRNA was localized with a cRNA probe corresponding to a 733-bp BamHI-HincII fragment of prodynorphin. kappa receptor-binding sites were labeled in one of two ways: [3H]U69,593 or [3H]bremazocine in the presence of a 300-fold excess of DAMGO and DPDPE. A high degree of correspondence between the kappa 1 receptor mRNA and kappa receptor binding was observed in several brain regions, including the endopiriform nucleus, claustrum, nucleus accumbens, olfactory tubercle, bed nucleus of the stria terminalis, medial preoptic area, paraventricular, supraoptic, suprachiasmatic, dorsomedial and ventromedial hypothalamic nuclei, basolateral, medial and cortical amygdaloid nuclei, midline thalamic nuclei, periaqueductal grey, parabrachial nucleus, locus coeruleus, and the nucleus of the solitary tract. Differences in the localization of kappa 1 receptor mRNA and binding and the relationship between the distribution of kappa 1 receptor and prodynorphin mRNAs are discussed.

Animals↗
PubMed1993

Increased mRNA accumulation in a psaB frame-shift mutant of Chlamydomonas reinhardtii suggests a role for translation in psaB mRNA stability.

Regulation of mRNA stability is an important control in the differential accumulation of chloroplast mRNAs that occurs in response to developmental and environmental signals. The mechanism by which differential mRNA accumulation is achieved is unknown. We have examined mRNA accumulation in a chloroplast mutant of Chlamydomonas reinhardtii previously shown to contain a single AT base-pair deletion in the psaB gene. In this mutant, steady-state levels of mRNA from psaB accumulate to a level more than twice that found in cells that have had the mutation repaired by chloroplast transformation. In vivo pulse labeling of RNA shows that increased mRNA accumulation is due to a more stable transcript. We show that inhibitors of chloroplast protein synthesis also increase mRNA accumulation from the psaB gene. The results are consistent with a link between polysome association, active synthesis and stability of psaB transcripts.

Animals↗
PubMed1997

Quantification of mRNA levels in joint capsule and articular cartilage of the murine knee joint by RT-PCR: kinetics of stromelysin and IL-1 mRNA levels during arthritis.

We developed a method to isolate well defined joint specimens from different compartments of normal and arthritic murine knee joints in which mRNA levels of stromelysin and IL-1 were semiquantified using RT-PCR. Joint capsule specimens were isolated on medial and lateral sides of the patella with a biopsy punch. Cartilage layers were isolated from patellae after a mild decalcification with EDTA. EDTA treatment had no effect on the amount and efficiency of amplification of mRNA when tested on isolated chondrocytes. After induction of experimental arthritis, stromelysin mRNA was elevated approximately 50 times in both joint capsule and cartilage. IL-1 was elevated 100 times in joint capsule but only 10 times in cartilage. Kinetic analysis of mRNA levels in cartilage during arthritis showed a prolonged elevation of stromelysin mRNA compared to IL-1. The variation in mRNA levels between joints of individual mice proved to be low, showing that sampling of the specimens and subsequent RT-PCR can be performed reliably. The current method offers a valuable approach to study gene expression in knee joints during murine experimental arthritis.

Animals↗
PubMed1991

Correlations between a nuclear and a mitochondrial mRNA of cytochrome c oxidase subunits, enzymatic activity and total mRNA content, in rat tissues.

Cytochrome c oxidase (COX), like other multi-subunit components of the respiratory chain, is controlled by both the nuclear and the mitochondrial genome. In order to find wether there is a close relationship between mRNAs encoded by the nucleus and by the mitochondrion, and between these mRNAs and enzyme activity, we compared six rat tissues (ventricle, liver, m. soleus, m. plantaris, and the white and red portions of m. gastrocnemius). We found a tenfold range for COX activity, a tenfold range for the contents of mRNA III (mitochondrial) and mRNA VIc (nuclear), a threefold range for total [poly(A)+] mRNA content and a sevenfold range for total RNA content in these tissues. The ratio of mRNA III to mRNA VIc was equal in each tissue, indicating the presence of a mechanism that coordinates the two genomes. There was a good correlation between mRNA content and COX activity (r = 0.78 for VIc, r = 0.77 for III; p less than 0.0001), demonstrating that the expression of this enzyme is mainly under pretranslational control.

Animals↗
PubMed1996

Enhanced expression of manganese superoxide dismutase mRNA and increased TNFalpha mRNA expression by gastric mucosa in gastric cancer.

Manganese superoxide dismutase (Mn-SOD), a mitochondrial enzyme, is a cytokine-regulated acute-phase protein that protects cells from free radicals. The current investigations examined the in vivo regulation of the expression of Mn-SOD mRNA and tumor necrosis factor alpha (TNFalpha) mRNA in gastric carcinoma tissue. The expression of these transcripts in breast carcinoma tissue also was examined because breast cancer is a much more TNF-sensitive tumor than gastric cancer. TNFalpha mRNA was markedly increased in gastric carcinoma tissue (p < 0.005). There were significantly higher levels of Mn-SOD mRNA in gastric carcinoma tissue than in noncancerous tissue (p < 0.0001). The level of Mn-SOD mRNA in gastric carcinoma tissue was higher than that in breast carcinoma tissue (p < 0.005). Up-regulation of Mn-SOD mRNA in gastric carcinoma tissue most likely serves as a protective mechanism against superoxide radicals and TNF cytotoxicity.

Adult↗
PubMed2002

Cellular localization of tumor necrosis factor-alpha mRNA and interleukin-6 mRNA in the rat liver after hemorrhagic shock.

PURPOSE: Our previous studies showed that tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 are induced after hemorrhagic shock and that their induction is attenuated by hyperbaric oxygen treatment. In this study, we tried to identify the cell types in the liver that are responsible for the increase in TNF-alpha mRNA and IL-6 mRNA after hemorrhage using in situ reverse transcription-polymerase chain reaction (in situ RT-PCR). METHODS: Chronically cannulated rats were subjected to hemorrhage, maintaining a mean arterial blood pressure of 40 mmHg for 1 h. They were resuscitated with the collected blood and saline, and the livers were removed at designated times, then fixed and frozen. RESULTS: Standard in situ hybridization could not detect the mRNAs of TNF-alpha and IL-6 in the livers; however, in situ RT-PCR detected TNF-alpha mRNA and IL-6 mRNA mainly in the vascular endothelial cells and perivascular nonparenchymal cells of the bled rats. Sinusoidal cells were positive for TNF-alpha mRNA, but negative for IL-6 mRNA. No signal was found in normal rats, or when the experimental protocol was modified to: omit the RT step; precede the RT step with RNA digestion; or use an irrelevant probe. CONCLUSION: These results show that vascular endothelial cells and perivascular nonparenchymal cells are activated after massive hemorrhage to produce inflammatory cytokines.

Animals↗
PubMed1992

Marked enhancement of acyl-CoA synthetase activity and mRNA, paralleled to lipoprotein lipase mRNA, in adipose tissues of Zucker obese rats (fa/fa).

To clarify the role of acyl-CoA synthetase in development of obesity, the mRNA levels and activities were studied in Zucker fatty rats (fa/fa). In Zucker fatty rats compared with their lean littermates, marked enhancement of ACS were observed in adipose tissues. Obese/lean rats ratio of ACS activity and mRNA in abdominal subcutaneous fat (3.3- and 3.9-fold, respectively) were greater than in mesenteric fat (2.0- and 2.2-fold). The enhancement of ACS activity and mRNA in the liver of fatty rats (1.2- and 1.8-fold) were less than those in the adipose tissues. There were no enhancement of ACS activities and mRNA levels in heart tissue of the obese rats. LPL mRNA levels were also enhanced in adipose tissue of fatty rats and obese/lean ratio of LPL mRNA was also higher in abdominal subcutaneous fat than mesenteric fat (6.2- vs 3.1-fold). The larger obese/lean rats ratio of LPL and ACS parameters in abdominal subcutaneous fat than mesenteric fat may be related to the observation that the increase of subcutaneous fat weight was larger than that of mesenteric fat weight in fatty rats (21.1- vs 4.9-fold). Integrated enhancement of LPL and ACS gene expression in adipose tissue may play an important role in the development of obesity.

Adipose Tissue↗