Lipoprotein Lipase mRNA Research Articles

Carnosic Acid Modulates Increased Hepatic Lipogenesis and Adipocytes Differentiation in Ovariectomized Mice Fed Normal or High-Fat Diets.

As postmenopausal women experience a rapid increase in cardiovascular disease (CVD) risk with an increase in abdominal fat, dietary interventions to reduce CVD risk have been emphasized. This study was aimed at investigating the effect of a high-fat diet (HFD) in combination with an ovariectomy on liver and adipose tissue fat metabolism. The efficacy of carnosic acid (CA) supplementation in the suppression of HFD- and ovariectomy-induced obesity was also evaluated. Ovariectomized (OVX) or sham-operated mice at eight weeks of age were fed with a normal diet (ND), HFD, ND and 0.02% CA, or HFD and 0.02% CA for 12 weeks. All of the animals were sacrificed at the age of 20 weeks. The blood and tissue markers of the lipogenesis and adipocyte differentiation were measured. As expected, ovariectomy decreased the uterus weight and serum 17β-estradiol concentration. The HFD and ovariectomy significantly contributed to increases in the body weight and total fat mass, which were effectively inhibited by CA supplementation. The circulating concentrations of insulin, leptin, and TG (triglyceride) were significantly higher in the HFD group, and the concentrations were two to five times higher in the OVX and HFD group compared with those of the ND group. The CA supplementation significantly lowered the insulin, leptin, and TG concentrations in the OVX and HFD mice. The hepatic protein expressions of pAMPK and pACC were up-regulated by CA supplementation in OVX mice fed either ND or HFD. The expressions of hepatic SREBP1c and FAS mRNA were the highest in the OVX and HFD group, which were suppressed by CA supplementation. The adipose tissue PPARγ, aP2, and lipoprotein lipase (LPL) mRNA expressions were up-regulated by a HFD or ovariectomy, while they were significantly reduced in the mice fed a CA supplemented diet. The TNF-α and IL-6 mRNA levels in the adipose tissue were decreased by providing CA in the OVX groups. These results suggest that HFD and ovariectomy independently contribute to body fat accumulation, and CA effectively alleviated the ovariectomy-induced increases in lipogenesis and adipocyte differentiation. Further human trials are required in order to evaluate the efficacy of rosemary-derive CA as natural anti-adipogenic compounds, especially in postmenopausal women.

PO-305 An 8-week, low carbohydrate, high fat, ketogenic diet enhanced exercise capacity through improved ketolysis and lipolysis in mice

PO-305 An 8-week, low carbohydrate, high fat, ketogenic diet enhanced exercise capacity through improved ketolysis and lipolysis in mice

Replacing fish oil with palm oil: Effects onmRNAexpression of fatty acid transport genes and signalling factors related to lipid metabolism in Nile tilapia (Oreochromis niloticus)

This study evaluated the effects of replacing fish oil (FO) with palm oil (PO) on enzyme activities and mRNA expression of lipid transport genes and signalling factors in juvenile Nile tilapia. Nile tilapia (9.34 ± 0.14 g) was fed five experimental diets with FO supplemented with PO at 0%, 25%, 50%, 75% and 100%. Liver was sampled from five fish per tank for analysis of fatty acids, enzyme activities and mRNA expression. Glucose 6‐phosphate dehydrogenase (G6PD) was highly expressed in groups fed higher levels of dietary PO, whilst liver X receptor (LXR) was highly expressed in groups fed lower levels of dietary PO. Groups fed 50% PO, 75% PO and 100% PO had significantly higher levels of G6PD mRNA expression whilst group fed 100% PO had significantly higher level of lipoprotein lipase (LPL) mRNA expression. Groups fed 75% PO and 100% PO recorded higher levels of PPAR‐α mRNA expression whilst higher level of malic enzyme mRNA expression was observed in group fed 75% PO. The mRNA expressions of the above stated genes and enzymes activities are predominantly influenced by dietary n‐3 PUFA and n‐6 PUFA levels. Dietary PO inclusion affected enzyme activities of LXR, PPAR‐α,PPAR‐β, LPL and FABP‐3. Activities of PPAR‐α, PPAR‐β and FABP‐3 were increased by PO inclusion whilst LXR and ELOVL 5 were reduced by PO inclusion. In conclusion, it could be inferred that substituting FO with PO could alter the metabolism pathway of genes such as LXR, G6PD, PPAR‐α, LPL and ME that are involved in the transport of fatty acids.

LPL protein in Chronic Lymphocytic Leukaemia have different origins in Mutated and Unmutated patients. Advances for a new prognostic marker in CLL.

Lipoprotein lipase (LPL) mRNA expression in chronic lymphocytic leukaemia (CLL) is associated with an unmutated immunoglobulin profile and poor clinical outcome. We evaluated the subcellular localization of LPL protein in CLL cells that did or did not express LPL mRNA. Our results show that LPL protein is differently located in CLL cells depending on whether it is incorporated from the extracellular medium in mutated CLL or generated de novo by leukaemic cells of unmutated patients. The specific quantification of endogenous LPL protein correlates with mRNA expression levels and mutational IGHV status, suggesting LPL protein as a possible reliable prognostic marker in CLL.

Effect of phytase enzyme on growth performance, serum biochemical alteration, immune response and gene expression in Nile tilapia

The present study aimed to investigate the effect of low phosphorus diet with or without different levels of phytase enzyme supplementation on growth performance, body composition, nutrient retention efficiency, gene expression, and health status of A. hydrophila challenged fish. A total of 240 monosex males of Nile tilapia (Oreochromis niloticus) with an average body weight of 23.19 ± 0.15 g/fish were used. Fish were randomly chosen and divided into 4 equal groups (60 fish per group), with 3 subgroups containing 20 fish as a replicate. Group 1, was fed on a diet containing 100% P, group 2, was fed on a diet containing 50% P, group 3 and 4, were fed on low P with 500 or 1000 units of phytase/Kg respectively. It was observed that the 50% phosphorus diet significantly reduced body weight, feed intake, feed conversion ratio (FCR), and protein efficiency ratio (PER) compared to Nile tilapia fish fed on the diet containing 100% phosphorus. In contrast, fish fed on the diet containing 50% phosphorus supplemented by 500 or 1000 phytase units/kg significantly (P ≤ 0.05) increased final body weight (FBW), total body gain (TBG), average daily gain (ADG), and weight gain compared to Nile tilapia fed on the same diet or fed on the diet containing normal phosphorus without phytase supplementation. Different phosphorus and phytase supplementation levels had no significant effect on serum total protein, albumin, and globulin concentrations, meanwhile, phytase supplementation increased serum calcium and phosphorus levels. Nile tilapia fed on phytase supplementation had an increase in body protein, lipid content, and nutrient utilization efficiency compared to Nile tilapia fed on the diet containing 100% phosphorus. Nile tilapia fed on low dietary phosphorus showed an increase in mortality after infection and a decrease in phagocytosis and neutrophil compared to fish fed on normal phosphorus. Phytase supplementation, made immune response parameters return to its normal values and the pathological lesions of liver, spleen, stomach, and intestine were reduced. Moreover, normal phosphorus significantly up-regulated lipoprotein lipase (LPL) mRNA expression and down-regulated fatty acid synthase (FAS) mRNA in Nile tilapia's liver while low phosphorus with or without phytase supplementation reduced LPL expression and relatively up-regulated FAS.

Breeding selection of rainbow trout for high or low muscle adiposity differentially affects lipogenic capacity and lipid mobilization strategies to cope with food deprivation

The present study evaluates the transcriptional regulation of lipid metabolism, adiponectin system and oxidative stress genes in two rainbow trout lines selected over seven generations for low (lean line, LL) or high (fat line, FL) muscle adiposity, and subjected to different fasting regimes. Under feeding conditions, FL fish had higher muscle lipid content, plasma triglycerides (TG) and non-esterified fatty acids (NEFAs) than the LL fish. Besides, FL fish had higher fatty acid synthase (fasn) mRNA levels in adipose tissue (AT) and white muscle (WM), and higher lipoprotein lipase (lpl) mRNA levels in WM, suggesting an increased lipogenic capacity and fatty acid uptake in the fatty genotype. In response to fasting, the two fish lines displayed a different trend in muscle lipid mobilization, plasma TG levels changes and lipid metabolism-related genes expression patterns. There were different fasn expression profiles between the fish lines in both, AT and WM, in agreement with the changes observed in plasma TG levels. The FL fish had higher adiponectin receptor 2 mRNA levels in WM and adiponectin mRNA levels in AT than LL fish after 1 and 4 weeks of fasting respectively, indicating a difference between genotypes in the adiponectin system. Furthermore, oxidative stress genes mRNA levels in both fish lines showed a different pattern between AT and WM upon fasting, probably indicating a higher protective effect in WM. Overall, the present study reveals a distinct metabolic regulation for each genotype, highlighting their different strategies in response to food deprivation.

Epigenetic Regulations of Genes Related to Lipid Metabolism by MicroRNA in Mice Fed High Fat Diet

BackgroundHigh fat diet impacts lipid metabolism by altering the transportation, oxidation, and storage of fatty acids. Lipoprotein lipase (LPL) plays a critical role in lipid metabolism by catalyzing triglyceride hydrolysis and lipoprotein uptake in multiple tissues. Previous study reported that miR‐29b negatively regulated LPL expression in mammary epithelial cells transfected with miR‐29b mimics. The present study investigated changes in LPL expression and epigenetic mechanisms by miR‐29 family in different tissues in mice fed a high fat diet.MethodFive‐week old male CBA mice were fed with either a control diet (Con group, 10% kcal from diet) or a high fat diet (HF group, 45% kcal from diet) ad libitum for 11 weeks.ResultsLPL mRNA was increased in adipose, muscle and colon in response to high fat diet. However, LPL mRNA expression decreased in the liver by high fat diet as well as hepatic lipase (HL). The results also showed the highest expression level of LPL mRNA in adipose tissue, followed by muscle, colon, and liver. Cpt1a mRNA, an important gene related to beta oxidation, was increased in adipose, muscle, colon, and liver in the HF group. Moreover, Cpt1a mRNA expression was the highest in liver followed by adipose, muscle, and colon. Meanwhile, high fat diet reduced the expression of miR‐29a, a predicted suppressor of LPL from miR‐29 family, in adipose tissue.ConclusionThe present results indicated that the triglyceride hydrolysis could be activated by high fat diet in other tissues than the liver and fatty acid transportation could be induced in mitochondria. Overall, LPL and Cpt1a mRNA changed differently in multiple tissue in response to high fat diet and is potentially post‐transcriptionally regulated by microRNA.Support or Funding InformationSource of research support (in a separate textbox): Campus Research Board of University of Illinois at Urbana‐Champaign and the USDA Cooperative State Research, Education and Extension Service, Hatch project numbers # ILLU‐698‐923 and ILLU‐698‐379This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Regulation of angiopoietin-like 4 and lipoprotein lipase in human adipose tissue

Elevated plasma triglycerides are increasingly viewed as a causal risk factor for coronary artery disease. One protein that raises plasma triglyceride levels and that has emerged as a modulator of coronary artery disease risk is angiopoietin-like 4 (ANGPTL4). ANGPTL4 raises plasma triglyceride levels by inhibiting lipoprotein lipase (LPL), the enzyme that catalyzes the hydrolysis of circulating triglycerides on the capillary endothelium. The objective of the present study was to assess the association between ANGPTL4 and LPL in human adipose tissue, and to examine the influence of nutritional status on ANGPTL4 expression. We determined ANGPTL4 and LPL mRNA and protein levels in different adipose tissue depots in a large number of severely obese patients who underwent bariatric surgery. Furthermore, in 72 abdominally obese subjects, we measured ANGPTL4 and LPL mRNA levels in subcutaneous adipose tissue in the fasted and postprandial state. ANGPTL4 mRNA levels were highest in subcutaneous adipose tissue, whereas LPL mRNA levels were highest in mesenteric adipose tissue. ANGPTL4 and LPL mRNA levels were strongly positively correlated in the omental and subcutaneous adipose tissue depots. In contrast, ANGPTL4 and LPL protein levels were negatively correlated in subcutaneous adipose tissue, suggesting a suppressive effect of ANGPTL4 on LPL protein abundance in subcutaneous adipose tissue. ANGPTL4 mRNA levels were 38% higher in the fasted compared to the postprandial state. Our data provide valuable insights into the relationship between ANGPTL4 and LPL in human adipose tissue, as well as the physiological function and regulation of ANGPTL4 in humans.

Magnolol-mediated regulation of plasma triglyceride through affecting lipoprotein lipase activity in apolipoprotein A5 knock-in mice.

Hyperlipidemia is a risk factor of arteriosclerosis, stroke, and other coronary heart disease, which has been shown to correlate with single nucleotide polymorphisms of genes essential for lipid metabolism, such as lipoprotein lipase (LPL) and apolipoprotein A5 (APOA5). In this study, the effect of magnolol, the main active component extracted from Magnolia officinalis, on LPL activity was investigated. A dose-dependent up-regulation of LPL activity, possibly through increasing LPL mRNA transcription, was observed in mouse 3T3-L1 pre-adipocytes cultured in the presence of magnolol for 6 days. Subsequently, a transgenic knock-in mice carrying APOA5 c.553G>T variant was established and then fed with corn oil with or without magnolol for four days. The baseline plasma triglyceride levels in transgenic knock-in mice were higher than those in wild-type mice, with the highest increase occurred in homozygous transgenic mice (106 mg/dL vs 51 mg/dL, p<0.01). After the induction of hyperglyceridemia along with the administration of magnolol, the plasma triglyceride level in heterozygous transgenic mice was significantly reduced by half. In summary, magnolol could effectively lower the plasma triglyceride levels in APOA5 c.553G>T variant carrier mice and facilitate the triglyceride metabolism in postprandial hypertriglyceridemia.

Intermittent Fasting Alleviates the Increase of Lipoprotein Lipase Expression in Brain of a Mouse Model of Alzheimer's Disease: Possibly Mediated by β-hydroxybutyrate.

Intermittent fasting has been demonstrated to protect against Alzheimer's disease (AD), however, the mechanism is unclear. Histone acetylation and lipoprotein lipase (LPL) are involved in AD progression. Importantly, LPL has been documented to be regulated by histone deacetylases (HDACs) inhibitors (increase histone acetylation level) in adipocyte and mesenchymal stem cells, or by fasting in adipose and muscle tissues. In brain, however, whether histone acetylation or fasting regulates LPL expression is unknown. This study was designed to demonstrate intermittent fasting may protect against AD through increasing β-hydroxybutyrate, a HDACs inhibitor, to regulate LPL. We also investigated microRNA-29a expression associating with regulation of LPL and histone acetylation. The results showed LPL mRNA expression was increased and microRNA-29a expression was decreased in the cerebral cortex of AD model mice (APP/PS1), which were alleviated by intermittent fasting. No significant differences were found in the total expression of LPL protein (brain-derived and located in capillary endothelial cells from peripheral tissues) in the cerebral cortex of APP/PS1 mice. Further study indicated that LPL located in capillary endothelial cells was decreased in the cerebral cortex of APP/PS1 mice, which was alleviated by intermittent fasting. LPL and microRNA-29a expression were separately increased and down-regulated in 2 μM Aβ25−35-exposed SH-SY5Y cells, but respectively decreased and up-regulated in 10 μM Aβ25−35-exposed cells, which were all reversed by β-hydroxybutyrate. The increase of HDAC2/3 expression and the decrease of acetylated H3K9 and H4K12 levels were alleviated in APP/PS1 mice by intermittent fasting treatment, as well in 2 or 10 μM Aβ25−35-exposed cells by β-hydroxybutyrate treatment. These findings above suggested the results from APP/PS1 mice were consistent with those from cells treated with 2 μM Aβ25−35. Interestingly, LPL expression was reduced (0.2-folds) and microRNA-29a expression was up-regulated (1.7-folds) in HDAC2-silenced cells, but respectively increased (1.3-folds) and down-regulated (0.8-folds) in HDAC3-silenced cells. Furthermore, LPL expression was decreased in cells treated with microRNA-29a mimic and increased with inhibitor treatment. In conclusion, intermittent fasting inhibits the increase of brain-derived LPL expression in APP/PS1 mice partly through β-hydroxybutyrate-mediated down-regulation of microRNA-29a expression. HDAC2/3 may be implicated in the effect of β-hydroxybutyrate on microRNA-29a expression.

Adipose Tissue LPL Methylation is Associated with Triglyceride Concentrations in the Metabolic Syndrome.

DNA methylation is one of the epigenetic mechanisms that regulate gene expression. DNA methylation may be modified by environmental and nutritional factors. Thus, epigenetics could potentially provide a mechanism to explain the etiology of metabolic disorders, such as metabolic syndrome (MetS). The aim of this study was to analyze the level of DNA methylation of several lipoprotein lipase (LPL)-promoter-CpG dinucleotides in a CpG island region and relate this to the gene and protein expression levels in human visceral adipose tissue (VAT) from individuals with and without MetS. VAT samples were collected from laparoscopic surgical patients without and with MetS, and levels of LPL mRNA, LPL protein, and LPL DNA methylation were measured by qPCR, western blot, and pyrosequencing. Biochemical and anthropometric variables were analyzed. Individuals included in a subset underwent a dietary fat challenge test, and levels of postprandial triglycerides were determined. We found higher levels of DNA methylation in MetS patients but lower gene expression and protein levels. There was a negative association between LPL methylation and LPL gene expression. We found a positive association between LPL methylation status and abnormalities of the metabolic profile and basal and postprandial triglycerides, whereas LPL gene expression was negatively associated with these abnormalities. We demonstrate that LPL methylation may be influenced by the degree of metabolic disturbances and could be involved in triglyceride metabolism, promoting hypertriglyceridemia and subsequent associated disorders, such as MetS.

Interscapular brown adipose tissue recruitment is hindered by a temperature environment of 33°C: Uncoupling protein-1 underexpression is not associated with obesity development in rats

Brown adipose tissue (BAT) generates heat due to unique thermogenic UC-mitochondria, an event known as nonshivering thermogenesis. Cold, adrenergic agents, hormones, etc., activate nonshivering thermogenesis, resulting in lipid mobilization, an increase in the mitochondria and mitochondrial cristae, and increased uncoupling protein-1 (UCP1) expression and its incorporation into mitochondrial cristae. BAT precursor cells mature and contribute to BAT growth in a process known as BAT recruitment. For the first time, we herein report the effect of a thermoneutral environment of 33?C on interscapular BAT (IBAT) in rats delivered and raised at 33?C. The control animals were housed at 20?C. Thermoneutral IBAT was atrophic (73 mg vs. 191 mg) but with more adipocyte precursor cells; euthermia (37.6?C) was maintained without nonshivering thermogenesis. Although IBAT was inactive, the thermoneutral animals did not develop obesity, and on the contrary, the thermoneutral environment of 33?C hindered the rats? growth, weight (65 gm vs. 139 gm), volume (67 gm vs.136 gm) and length (12 cm vs. 16 cm). The thermoneutral brown adipocytes were smaller (7234 ?m3 vs. 9198 ?m3) with more lipids (4919 ?m3 vs. 4507 ?m3) and a smaller mitochondrial cristae area (52504 ?m2 vs. 61288 ?m2/adipocyte). Lipoprotein lipase mRNA expression was 11% (vs. 58% in control) and UCP1 mRNA expression was 34% (vs. 93% control). UCP1 immunoelectron microscopic study detected 160 UCP1-gold particles (vs. 700 in control) per UC-mitochondrion; thermoneutral brown adipocytes had 9-fold fewer UCP1-gold particles (0.34x106 vs. 2.99x106 UCP1-gold particles), and thermoneutral UC-mitochondria developed specific intramitochondrial tubular inclusions.

Effects of branched-chain volatile fatty acids on lactation performance and mRNA expression of genes related to fatty acid synthesis in mammary gland of dairy cows

Branched-chain volatile fatty acids (BCVFA) supplements could promote lactation performance and milk quality by improving ruminal fermentation and milk fatty acid synthesis. This study was conducted to evaluate the effects of BCVFA supplementation on milk performance, ruminal fermentation, nutrient digestibility and mRNA expression of genes related to fatty acid synthesis in mammary gland of dairy cows. A total of 36 multiparous Chinese Holstein cows averaging 606±4.7 kg of BW, 65±5.2 day in milk (DIM) with daily milk production of 30.6±0.72 kg were assigned to one of four groups blocked by lactation number, milk yield and DIM. The treatments were control, low-BCVFA (LBCVFA), medium-BCVFA (MBCVFA) and high-BCVFA (HBCVFA) with 0, 30, 60 and 90 g BCVFA per cow per day, respectively. Experimental periods were 105 days with 15 days of adaptation and 90 days of data collection. Dry matter (DM) intake tended to increase, but BW changes were similar among treatments. Yields of actual milk, 4% fat corrected milk, milk fat and true protein linearly increased, but feed conversion ratio (FCR) linearly decreased with increasing BCVFA supplementation. Milk fat content linearly increased, but true protein content tended to increase. Contents of C4:0, C6:0, C8:0, C10:0, C12:0, C14:0 and C15:0 fatty acids in milk fat linearly increased, whereas other fatty acids were not affected with increasing BCVFA supplementation. Ruminal pH, ammonia N concentration and propionate molar proportion linearly decreased, but total VFA production and molar proportions of acetate and butyrate linearly increased with increasing BCVFA supplementation. Consequently, acetate to propionate ratios linearly increased. Digestibilities of DM, organic matter, CP, NDF and ADF also linearly increased. In addition, mRNA expressions of peroxisome proliferator-activated receptor γ, sterol regulatory element-binding factor 1 and fatty acid-binding protein 3 linearly increased, mRNA expressions of acetyl-coenzyme A carboxylase-α, fatty acid synthase and stearoyl-CoA desaturase quadratically increased. However, lipoprotein lipase mRNA expression was not affected by treatments. The results indicated that lactation performance and milk fat synthesis increased with BCVFA supplementation by improving ruminal fermentation, nutrient digestibility and mRNA expressions of genes related to milk fat synthesis.

ANGPTL3 is part of the machinery causing dyslipidemia majorily via LPL inhibition in mastitis mice

Previous investigations have shown that inflammation induces changes in lipid and lipoprotein metabolism, and increased expression of angiopoietin-like protein 3 (ANGPTL3) contributes to the development of dyslipidemia. Here we investigated whether there is a correlation between increased ANGPTL3 expression and dyslipidemia in mastitis mice. Thirty mice were divided into two groups: control group and Staphylococcus aureus (S. aureus)–induced mastitis mice group. Changes in the levels of blood lipids [total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C)]; activity of myeloperoxidase (MPO); concentrations of plasma inflammation biomarkers [interferon-γ (IFNγ), tumor necrosis factor α (TNFα), and interleukin-1α (IL-1α)]; concentration of plasma ANGPTL3 protein; lipoprotein lipase (LPL) activities in postheparin plasma; expressions of hepatic N-acetylgalactosaminyltransferase 2 (GALNT2), hepatic ANGPTL3 and adipose LPL were determined. The major results indicated specific pathological mammary tissue changes, elevated MPO activity, reduced GALNT2 mRNA expression, elevated ANGPTL3 mRNA and protein expression and reduced LPL mRNA and protein expression. In plasma samples the S.aureus infused mice displayed elevated ANGPTL3 protein concentration, TG, TC and LDL-C levels, and reduced postheparin LPL activities and HDL-C level. The data suggests that ANGPTL3 is part of the machinery causing dyslipidemia majorily via LPL inhibition in mastitis mice.

Decreased lipogenesis-promoting factors in adipose tissue in postmenopausal women with overweight on a Paleolithic-type diet

PurposeWe studied effects of diet-induced postmenopausal weight loss on gene expression and activity of proteins involved in lipogenesis and lipolysis in adipose tissue.MethodsFifty-eight postmenopausal women with overweight (BMI 32.5 ± 5.5) were randomized to eat an ad libitum Paleolithic-type diet (PD) aiming for a high intake of protein and unsaturated fatty acids or a prudent control diet (CD) for 24 months. Anthropometry, plasma adipokines, gene expression of proteins involved in fat metabolism in subcutaneous adipose tissue (SAT) and lipoprotein lipase (LPL) activity and mass in SAT were measured at baseline and after 6 months. LPL mass and activity were also measured after 24 months.ResultsThe PD led to improved insulin sensitivity (P < 0.01) and decreased circulating triglycerides (P < 0.001), lipogenesis-related factors, including LPL mRNA (P < 0.05), mass (P < 0.01), and activity (P < 0.001); as well as gene expressions of CD36 (P < 0.05), fatty acid synthase, FAS (P < 0.001) and diglyceride acyltransferase 2, DGAT2 (P < 0.001). The LPL activity (P < 0.05) and gene expression of DGAT2 (P < 0.05) and FAS (P < 0.05) were significantly lowered in the PD group versus the CD group at 6 months and the LPL activity (P < 0.05) remained significantly lowered in the PD group compared to the CD group at 24 months.ConclusionsCompared to the CD, the PD led to a more pronounced reduction of lipogenesis-promoting factors in SAT among postmenopausal women with overweight. This could have mediated the favorable metabolic effects of the PD on triglyceride levels and insulin sensitivity.

Role of RNA-binding protein HuR in human adipocyte differentiation

Objective To investigate the expressions of RNA-binding protein human antigen R(HuR), fatty acid binding protein type 4(FABP4), fatty acid synthetase(FASN), and lipoprotein lipase(LPL)during the differentiation of human adipocytes, and to explore their possible roles. Methods Human adipose-derived mesenchymal stem cells were induced by adipogenic differentiation, and the adipogenesis of cells was observed by oil red O staining. The expressions of HuR, FABP4, FASN, and LPL mRNA and protein were detected by real-time PCR and Western blotting. After HuR was silenced by siRNA, the change of adipogenesis for human adipose-derived mesenchymal stem cells was observed and the expressions of adipogenic genes were detected. Results The expressions of HuR, FABP4, FASN, and LPL mRNA and protein were significantly increased after human adipose-derived mesenchymal stem cells were induced to differentiate into adipocytes(all P<0.01). After HuR expression was down-regulated by siRNA, the adipogenic level of human adipose-derived mesenchymal stem cells was reduced, with decreased protein levels of FABP4, FASN, and LPL(all P<0.05), which were without changes for their mRNA levels. Conclusion HuR promotes the differentiation of human adipocytes mainly via regulating the changes of FABP4, FASN, and LPL protein levels. (Chin J Endocrinol Metab, 2017, 33: 854-860) Key words: Adipocyte differentiation; RNA binding protein; Human antigen R; Adipocyte fatty acid binding protein; Fatty acid synthase; Lipoprotein lipase

Tenomodulin is essential for prevention of adipocyte accumulation and fibrovascular scar formation during early tendon healing

Tenomodulin (Tnmd) is the best-known mature marker for tendon and ligament lineage cells. It is important for tendon maturation, running performance and has key implications for the resident tendon stem/progenitor cells (TSPCs). However, its exact functions during the tendon repair process still remain elusive. Here, we established an Achilles tendon injury model in a Tnmd knockout (Tnmd−/−) mouse line. Detailed analyses showed not only a very different scar organization with a clearly reduced cell proliferation and expression of certain tendon-related genes, but also increased cell apoptosis, adipocyte and blood vessel accumulation in the early phase of tendon healing compared with their wild-type (WT) littermates. In addition, Tnmd−/− tendon scar tissue contained augmented matrix deposition of biglycan, cartilage oligomeric matrix protein (Comp) and fibronectin, altered macrophage profile and reduced numbers of CD146-positive cells. In vitro analysis revealed that Tnmd−/− TSPCs exhibited significantly reduced migration and proliferation potential compared with that of WT TSPCs. Furthermore, Tnmd−/− TSPCs had accelerated adipogenic differentiation accompanied with significantly increased peroxisome proliferator-activated receptor gamma (Pparγ) and lipoprotein lipase (Lpl) mRNA levels. Thus, our results demonstrate that Tnmd is required for prevention of adipocyte accumulation and fibrovascular scar formation during early tendon healing.

Cloning and characterization of lipoprotein lipase (LPL) and the effects of dietary lipid levels on the expression of LPL in the redlip mullet (Liza haematocheila)

The genetic improvement of redlip mullet Liza haematocheila through breeding programmes is of interest for this important aquaculture species. Lipoprotein lipase (LPL) is a key enzyme in lipid deposition and metabolism. The purpose of this study was to investigate the nutritional regulation of LPL in redlip mullet. We cloned and identified the LPL gene, determined LPL gene expression in various tissues, and examined the effect of dietary lipid level on hepatic LPL gene expression. The LPL gene of redlip mullet Liza haematocheila (L.hLPL) was 2,395 bp in length and encoded 516 amino acids. Sequence analysis showed that L.hLPL shared 61%–90.3% identity with LPLs in other species. Expression patterns of hepatic L.hLPL were studied in redlip mullet fed diets containing 2.0, 4.8, 7.5, 9.8, 12.0 or 14.6 g/kg, crude fat for 60 days by real‐time quantitative PCR. The abundance of LPL mRNA in hepatic tissue increased with the increase in dietary fat. The expression L.hLPL mRNA was significantly higher in the groups fed diets with 14.6 and 12.0 g/kg fat than in the other groups (p < .05). Gene expression was significantly higher in the abdominal fat of redlip mullet (p < .05) compared with other tissues. In conclusion, a high fat diet (9.79–14.59 g/kg) induces L.hLPL expression in abdominal fat.

Effects of chromium picolinate on fat deposition, activity and genetic expression of lipid metabolism-related enzymes in 21 day old Ross broilers.

ObjectiveThis experiment was conducted to investigate the effects of chromium picolinate (CrP) on fat deposition, genetic expression and enzymatic activity of lipid metabolism-related enzymes.MethodsTwo hundred forty one-day-old Ross broilers were randomly divided into 5 groups with 4 replicates per group and 12 Ross broiler chicks per replicate. The normal control group was fed a basal diet, and the other groups fed the same basal diet supplemented with 0.1, 0.2, 0.4, and 0.8 mg/kg CrP respectively. The experiment lasted for 21 days.ResultsAdded CrP in the basal diet decreased the abdominal fat, had no effects on subcutaneous fat thickness and inter-muscular fat width; 0.2 mg/kg CrP significantly decreased the fatty acid synthase (FAS) enzymatic (p<0.05); acetyl-CoA carboxylase (ACC) enzymatic activity decreased in all CrP groups (p<0.05); hormone-sensitive lipase (HSL) enzymatic activity also decreased, but the change was not significant (p>0.05); 0.4 mg/kg CrP group significantly decreased the lipoprotein lipase (LPL) enzymatic activity. FAS mRNA expression increased in all experimental groups, and the LPL mRNA expression significantly increased in all experimental groups (p<0.05), but not 0.2 mg/kg CrP group.ConclusionThe results indicated that adding CrP in basal diet decreased the abdominal fat percentage, had no effects on subcutaneous fat thickness and inter-muscular fat width, decreased the enzymatic activity of FAS, ACC, LPL and HSL and increased the genetic expression levels of FAS and LPL.

Placental lipoprotein lipase DNA methylation alterations are associated with gestational diabetes and body composition at 5 years of age

ABSTRACTGestational diabetes mellitus (GDM) is associated with obesity in childhood. This suggests that consequences of in utero exposure to maternal hyperglycemia extend beyond the fetal development, possibly through epigenetic programming. The aims of this study were to assess whether placental DNA methylation (DNAm) marks were associated with maternal GDM status and to offspring body composition at 5 years old in a prospective birth cohort. DNAm levels were measured in the fetal side of the placenta in 66 samples (24 from GDM mothers) using bisDNA-pyrosequencing. Anthropometric and body composition (bioimpedance) were measured in children at 5 years of age. Mann-Whitney and Spearman tests were used to assess associations between GDM, placental DNAm levels at the lipoprotein lipase (LPL) locus and children's weight, height, body mass index (BMI), body fat, and lean masses at 5 years of age. Weight, height, and BMI z-scores were computed according to the World Health Organization growth chart. Analyses were adjusted for gestational age at birth, child sex, maternal age, and pre-pregnancy BMI. LPL DNAm levels were positively correlated with birth weight z-scores (r = 0.252, P = 0.04), and with mid-childhood weight z-scores (r = 0.314, P = 0.01) and fat mass (r = 0.275, P = 0.04), and negatively correlated with lean mass (r = −0.306, P = 0.02). We found a negative correlation between LPL DNAm and mRNA levels in placenta (r = −0.459; P < 0.001), which highlights the regulation of transcriptional activity by these epivariations. We demonstrated that alterations in fetal placental DNAm levels at the LPL gene locus are associated with the anthropometric profile in children at 5 years of age. These findings support the concept of fetal metabolic programming through epigenetic changes.