Lipid Deposition In Muscle Research Articles

Protaetia brevitarsis Hydrolysate Mitigates Muscle Dysfunction and Ectopic Fat Deposition Triggered by a High-Fat Diet in Mice.

Obesity is a key factor in metabolic syndrome (MetS) development. Consumption of a high-fat diet (HFD) accelerates the onset of obesity and associated metabolic complications. Protaetia brevitarsis (PB) has been traditionally utilized in Korean medicine for its antioxidant, anti-diabetic, anticancer, and hepatoprotective effects. However, specific effects of PB hydrolysate on skeletal muscles have not been fully elucidated. Therefore, this study sought to assess the influence of PB on HFD-induced MetS, focusing on the lipid metabolism and inflammatory responses mediated by AMP-activated protein kinase activation. To induce obesity, 6-week-old C57BL/6J mice were maintained on an HFD for 8 weeks, after which PB hydrolysate was orally administered for 16 weeks while the HFD regimen was sustained. A glucose tolerance test was conducted orally to evaluate glucose regulation, and forelimb grip strength was assessed upon completion of the experimental period. Histological assessments, serum biochemical analysis, lipid extraction, Western blot analysis, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) were performed following euthanasia. PB significantly reduced ectopic lipid deposition in skeletal muscles, enhanced muscle strength, and improved insulin sensitivity by increasing fatty acid oxidation via AMP-activated protein kinase/carnitine palmitoyltransferase 1 activation and inhibiting lipogenesis via stearoyl-CoA desaturase 1 gene downregulation. Furthermore, PB alleviated HFD-induced low-grade chronic inflammation by decreasing systemic monocyte chemoattractant protein 1 levels, thereby reducing ectopic fat deposition. This study highlights the potential of PB as a nutraceutical to mitigate MetS in HFD-fed mice.

Comparative lipidomic and metabolomic profiling of mdx and severe mdx-apolipoprotein e-null mice

AbstractDespite its notoriously mild phenotype, the dystrophin-deficient mdx mouse is the most common model of Duchenne muscular dystrophy (DMD). By mimicking a human DMD-associated metabolic comorbidity, hyperlipidemia, in mdx mice by inactivating the apolipoprotein E gene (mdx-ApoE) we previously reported severe myofiber damage exacerbation via histology with large fibro-fatty infiltrates and phenotype humanization with ambulation dysfunction when fed a cholesterol- and triglyceride-rich Western diet (mdx-ApoEW). Herein, we performed comparative lipidomic and metabolomic analyses of muscle, liver and serum samples from mdx and mdx-ApoEW mice using solution and high-resolution-magic angle spinning (HR-MAS) 1H-NMR spectroscopy. Compared to mdx and regular chow-fed mdx-ApoE mice, we observed an order of magnitude increase in lipid deposition in gastrocnemius muscle of mdx-ApoEW mice including 11-fold elevations in -CH3 and -CH2 lipids, along with pronounced elevations in serum cholesterol, fatty acid, triglyceride and phospholipids. Hepatic lipids were also elevated but did not correlate with the extent of muscle lipid infiltration or differences in serum lipids. This study provides the first lipometabolomic signature of severe mdx lesions exacerbated by high circulating lipids and lends credence to claims that the liver, the main regulator of whole-body lipoprotein metabolism, may play only a minor role in this process.

Fucoxanthin Mitigates High-Fat-Induced Lipid Deposition and Insulin Resistance in Skeletal Muscle through Inhibiting PKM1 Activity.

Glucose and lipid metabolism dysregulation in skeletal muscle contributes to the development of metabolic disorders. The efficacy of fucoxanthin in alleviating lipid metabolic disorders in skeletal muscle remains poorly understood. In this study, we systematically investigated the impact of fucoxanthin on mitigating lipid deposition and insulin resistance in skeletal muscle employing palmitic acid-induced lipid deposition in C2C12 cells and ob/ob mice. Fucoxanthin significantly alleviated PA-induced skeletal muscle lipid deposition and insulin resistance. In addition, fucoxanthin prominently upregulated the expression of lipid metabolism-related genes (Pparα and Cpt-1), promoting fatty acid β-oxidation metabolism. Additionally, fucoxanthin significantly increased the expression of Pgc-1α and Tfam, elevated the mtDNA/nDNA ratio, and reduced ROS levels. Further, we identified pyruvate kinase muscle isozyme 1 (PKM1) as a high-affinity protein for fucoxanthin by drug affinity-responsive target stability and LC-MS and confirmed their robust interaction by CETSA, microscale thermophoresis, and circular dichroism. Supplementation with pyruvate, the product of PKM1, significantly attenuated the beneficial effects of fucoxanthin on lipid deposition and insulin resistance. Mechanistically, fucoxanthin reduced glucose glycolysis rate and enhanced mitochondrial biosynthesis and fatty acid β-oxidation through inhibiting PKM1 activity, thereby alleviating lipid metabolic stress. These findings present a novel clinical strategy for treating metabolic diseases using fucoxanthin.

Cold exposure affects glucose metabolism, lipid droplet deposition and mitophagy in skeletal muscle of newborn goats

Cold exposure is a common stressor for newborn goats. Skeletal muscle plays an important role in maintaining whole-body homeostasis of glucose and lipid metabolism. However, the molecular mechanisms underlying regulation of skeletal muscle of newborn goats by cold exposure remains unclear. In this study, we found a significant increase (P < 0.01) in serum glucagon levels after 24 h of cold exposure (COLD, 6°C), while glucose and insulin concentrations were significantly decreased (P < 0.01) compared to room temperature (RT, 25°C). Additionally, we found that cold exposure reduced glycogen content (P < 0.01) in skeletal muscle. Pathway enrichment analysis revealed that cold exposure activated skeletal muscle glucose metabolism pathways (including insulin resistance and the insulin signaling pathway) and mitophagy-related pathways. Cold exposure up-regulated the expression of genes involved in fatty acid and triglyceride synthesis, promoting skeletal muscle lipid deposition. Notably, cold exposure induced mitophagy in skeletal muscle.

Transcriptome profiling of longissimus dorsi during different prenatal stages to identify genes involved in intramuscular fat deposition in lean and obese pig breeds

BackgroundThere was significant difference in muscle development between fat-type and lean-type pig breeds.Methods and resultsIn current study, transcriptome analysis and bioinformatics analysis were used to compare the difference in longissimus dorsi (LD) muscle at three time-points (38 days post coitus (dpc), 58 dpc, and 78 dpc ) between Huainan (HN) and Large white (LW) pig breeds. A total of 24500 transcripts were obtained in 18 samples, and 2319, 2799, and 3713 differently expressed genes (DEGs) were identified between these two breeds at 38 dpc, 58 dpc, and 78 dpc, respectively. And the number and foldchange of DEGs were increased, the alternative splice also increased. The cluster analysis of DEGs indicated the embryonic development progress of LD muscle between these two breeds was different. There were 539 shared DEGs between HN and LW at three stages, and the top-shared DEGs were associated with muscle development and lipid deposition, such as KLF4, NR4A1, HSP70, ZBTB16 and so on.ConclusionsThe results showed DEGs between Huainan (HN) and Large white (LW) pig breeds, and contributed to the understanding the muscle development difference between HN and LW, and provided basic materials for improvement of meat quality.

STC2 Inhibits Hepatic Lipid Synthesis and Correlates with Intramuscular Fatty Acid Composition, Body Weight and Carcass Traits in Chickens

Stanniocalcin 2 (STC2) is a secreted glycoprotein involved in multiple biological processes. To systemically study the biological role of STC2 in chickens, phylogenetic tree analysis and conservation analysis were conducted. Association analysis between variations in the STC2 gene and the economic traits of Gushi-Anka F2 was conducted. The tissue expression patterns of STC2 expression in different chicken tissues and liver at different stages were detected. The biological role of STC2 in chicken liver was investigated through overexpression and interfering methods in the LMH cell line. Correlation analyses between STC2 expression and lipid components were conducted. (1) The phylogenetic tree displayed that chicken STC2 is most closely related with Japanese quail and most distantly related with Xenopus tropicalis. STC2 has the same identical conserved motifs as other species. (2) rs9949205 (T &gt; C) found in STC2 intron was highly significantly correlated with chicken body weight at 0, 2, 4, 6, 8, 10 and 12 weeks (p &lt; 0.01). Extremely significant correlations of rs9949205 with semi-evisceration weight (SEW), evisceration weight (EW), breast muscle weight (BMW), leg muscle weight (LMW), liver weight and abdominal fat weight (AFW) were revealed (p &lt; 0.01). Significant associations between rs9949205 and abdominal fat percentage, liver weight rate, breast muscle weight rate and leg muscle weight rate were also found (p &lt; 0.05). Individuals with TT or TC genotypes had significantly lower abdominal fat percentage and liver weight rate compared to those with the CC genotype, while their body weight and other carcass traits were higher. (3) STC2 showed a high expression level in chicken liver tissue, which significantly increased with the progression of age (p &lt; 0.05). STC2 was observed to inhibit the content of lipid droplets, triglycerides (TG) and cholesterol (TC), as well the expression level of genes related to lipid metabolism in LMH cells. (4) Correlation analysis showed that the STC2 gene was significantly correlated with 176 lipids in the breast muscle (p &lt; 0.05) and mainly enriched in omega-3 and omega-6 unsaturated fatty acids. In conclusion, the STC2 gene in chicken might potentially play a crucial role in chicken growth and development, as well as liver lipid metabolism and muscle lipid deposition. This study provides a scientific foundation for further investigation into the regulatory mechanism of the STC2 gene on lipid metabolism and deposition in chicken liver.

Identification and functional prediction of lncRNAs associated with intramuscular lipid deposition in Guangling donkeys.

Many studies have shown that long non-coding RNAs (lncRNAs) play key regulatory roles in various biological processes. However, the importance and molecular regulatory mechanisms of lncRNAs in donkey intramuscular fat deposition remain to be further investigated. In this study, we used published transcriptomic data from the longissimus dorsi muscle of Guangling donkeys to identify lncRNAs and obtained 196 novel lncRNAs. Compared with the coding genes, the novel lncRNAs and the known lncRNAs exhibited some typical features, such as shorter transcript length and smaller exons. A total of 272 coding genes and 52 lncRNAs were differentially expressed between the longissimus dorsi muscles of the low-fat and high-fat groups. The differentially expressed genes were found to be involved in various biological processes related to lipid metabolism. The potential target genes of differentially expressed lncRNAs were predicted by cis and trans. Functional analysis of lncRNA targets showed that some lncRNAs may act on potential target genes involved in lipid metabolism processes and regulate lipid deposition in the longissimus dorsi muscle. This study provides valuable information for further investigation of the molecular mechanisms of lipid deposition traits in donkeys, which may improve meat traits and facilitate the selection process of donkeys in future breeding.

Kallstatin/Serpina3c improves hyperlipidemia induced by high-fat diet via regulating glycolipid metabolism in adipose tissue

Abstract Background Hyperlipidemia is an independent risk factor for cardiovascular diseases. Studies showed that the plasma Kallstatin (KS) in obese patients was reduced, and the decreased KS in obese patients with type 2 diabetes was increased after weight loss. The mouse homologous gene of human KS is Serpina3c, and the relationship between KS/Serpina3c and hyperlipidemia and its regulatory mechanism are unclear. Purpose To explore whether KS/Serpina3c improves hyperlipidemia and specific mechanisms. Methods The serum KS level of Chinese hyperlipidemia population was detected by ELISA. Serpina3c knockout mice (Serpina3c KO) were constructed based on the strategy of Cre/loxP recombination system. The adipocyte-specific Serpina3c knockout adeno-associated virus (AAV8-shSerpina3c) and control (AAV8-shNC) were constructed, and the adipocyte-specific Serpina3c overexpression adeno-associated virus (AAV8-Serpina3c) were constructed. The 8-week-old C57BL/6J mice were injected with AAV8-shSerpina3c or AAV8-shNC in situ into the inguinal adipose tissue (iWAT). Serpina3c KO mice were injected with AAV8-Serpina3c or AAV8-shNC in situ into the iWAT. The mice model of hyperlipidemia was established by feeding high-fat diet (HFD) for 16 weeks. The fat content of mice was observed with 7.0T magnetic resonance imaging (MRI)system. The serum triglyceride, total cholesterol, LDL and HDL were detected with the kit. Serpina3c KD, Serpina3c OV or control 3T3-L1 adipocytes were stimulated by PA for RNA-seq. Results (1) The serum KS decreased in hyperlipidemic people in China. (2) The 7.0T MRI system displayed bigger fat in the Serpina3c KO mice and AAV8-shSerpina3c mice. (4) The serum results showed higher lipids in Serpina3c KO and AAV8-shSerpina3c mice. (5) Oil red O staining showed increased lipid deposition in liver, muscle and heart. (6) The RNA-seq results revealed that the HIF1α and glycolysis pathways of Serpina3c KD adipocyte increased, while the fatty acid metabolic pathway decreased. The results of primary adipocytes verified the increase of glycolysis and decreased β oxidation. (7) And the fatty acid uptake in liver, heart and muscle tissue of Serpina3c KO mice and AAV8-shSerpina3c mice increased, and the β oxidation decreased. Conclusions The expression and secretion of KS/Serpina3c decreased in HFD adipose, which promotes glycolysis and inhibits fatty acids β oxidation of adipocytes. On the one hand, the decrease of Serpina3c activates glycolysis and increases the production of glycerol 3-phosphate by activating HIF1α. On the other hand, CPT1 was inhibited by increased HIF1α, impeding the activated fatty acid (Fatty-acyl-CoA) in the cytoplasm entering the mitochondria through CPT1. Glycerol 3-phosphate and fatty acyl CoA accumulated in the cytoplasm of adipocyte synthesize triglycerides through the diglyceride pathway, aggravating hyperlipidemia induced by HFD.Schematic diagram

Ectopic lipid deposition in muscle and liver, quantified by proton magnetic resonance spectroscopy.

Advances in the development of noninvasive imaging techniques have spurred investigations into ectopic lipid deposition in the liver and muscle and its implications in the development of metabolic diseases such as type 2 diabetes. Computed tomography and ultrasound have been applied in the past, though magnetic resonance-based methods are currently considered the gold standard as they allow more accurate quantitative detection of ectopic lipid stores. This reviewfocuses on methodological considerations of magnetic resonance-based methods to image hepatic and muscle fat fractions, and it emphasizes anatomical and morphological aspects and how these may influence data acquisition, analysis, and interpretation.

Muscular lipidomics and transcriptomics reveal the effects of bile acids on lipid metabolism in high-fat diet-fed grouper.

Little information is available on how exogenous bile acids alter lipid metabolism in muscle of fish. In the present study, an 8-week feeding trial were used to investigate the impacts of bile acids on lipid deposition, lipid metabolism, lipidomics, and transcriptomics in muscle of pearl gentian grouper (Epinephelus fuscoguttatus♀ × E. lanceolatus♂) fed a high-fat diet (HD). The HD treatment significantly increased the crude lipid content, while bile acids diet (BD) treatment decreased it (p = 0.057). BD treatment significantly decreased triglycerides level and significantly increased phosphatidylcholines, phosphatidylethanolamines, and phosphatidylglycerol levels. The contents of TG (17:0/18:2/18:2), TG (17:1/18:2/22:6), PC (6:0/22:1), PC (9:0/26:1), PC (26:1/6:0), PC (17:2/18:2), PE (16:0/18:1), PE (18:0/17:1), PG (18:0/20:5), PG (18:3/20:5), PG (19:0/16:1), and PG (18:0/18:1) in muscle were well response to dietary lipid level and bile acids supplementation. HD and BD groups induced a variety of adaptive metabolic responses in transcriptomics. HD treatment increased the lipogenesis and decreased lipolysis, whereas BD treatment decreased the lipogenesis and increased lipolysis. Present study revealed the improvement of muscular lipid metabolism and lipid composition in response to bile acids administration in pearl gentian grouper.

The Mef2c/AdipoR1 axis is responsible for myogenic differentiation and is regulated by resistin in skeletal muscles

Previous studies have shown that accumulated lipid and insulin resistance emerges in skeletal muscle after the onset of obesity and diabetes. We have previously shown that resistin significantly increases lipid contents in C2C12 cells. However, studies evaluating the effects of resistin on skeletal muscle cells and tissues are limited; despite that, an understanding of resistin action and function on lipid alteration in skeletal muscle tissues is critical for understanding obesity-related diseases. In this study, we document that resistin increases lipid deposition both in vitro and in vivo. Further, resistin promotes fiber type transformation, decreases enzyme activities, inhibits myogenic differentiation, and decreases muscle grip and excise endurance. In addition, adiponectin signaling is activated during myocyte differentiation, but it is inhibited at elevated resistin concentrations. Mechanistic investigation revealed that mef2c is responsible for adiponectin signaling pathway inhibition by inhibiting adipoR1 expression at the transcriptional level. In conclusion, this is the first study to document that resistin increases ectopic lipid deposition in skeletal muscles via a mef2c-adipoR1 signaling pathway, which reveals for the first time the presence of crosstalk between resistin and adiponectin in skeletal muscles.

Preferential deposition of dairy derived fatty acids in muscle tissue is partially due to the upregulation of CD36 in a low-birth-weight swine model.

Metabolic syndrome is a worldwide health issue. Previous research has revealed that low-birth weight (LBW) swine fed a high-fat (HF) diet were susceptible to insulin resistance (IR) and developed a preferential intestinal lipid absorption, hypertriglyceridemia, and muscle steatosis. We hypothesized that fatty acid transporters such as CD36, FATP4, and FABP2 could potentially explain the development of these conditions. In addition, dairy-derived fatty acids have been shown to be valid biomarkers to assess dairy intake, which can be utilized to investigate muscle lipid deposition in LBW swine. The overall aim of this study was to delineate molecular transport candidates responsible for intestinal lipid absorption and muscle lipid deposition in LBW swine; and secondly to determine what dietary fatty acids might accumulate preferentially in pork muscle when consuming dairy products. At 5 weeks of age, normal birth weight (NBW) and LBW piglets were randomly assigned to three experimental diets: 1-chow diet, 2-HF diet, or 3-isocaloric HF diet supplemented with full fat dairy products. At 12 weeks of age, piglets were euthanized, and carcass, fasting plasma, biceps femoris and jejunum mucosal scrapings were collected. Results showed that HF-fed LBW swine exhibited early signs of IR (fasting glucose, P < 0.05; fasting insulin, P = 0.091; HOMA-IR, P = 0.086) compared with NBW-Chow, which were attenuated with increased dairy intake. Muscle samples from HF-fed LBW swine contained significantly more triglyceride compared to Chow-fed NBW swine (P < 0.05). Increased dairy intake significantly increased myristic acid (C14:0) and DPA (C22:5n3) relative to HF feeding alone (P < 0.05). All HF-fed LBW swine (regardless of dairy intake) exhibited an upregulation of CD36 expression (but not FABP2) compared with NBW littermates in both the small intestine and muscle (P < 0.05). Interestingly, increased dairy intake significantly increased the Canadian Lean Yield percentage in LBW swine fed an HF diet (P < 0.05). Findings from this study provide evidence on the mechanistic pathway of intestinal and muscle lipid metabolism in an innovative LBW swine model. We have also revealed that increasing dairy intake can enhance the incorporation of dietary long-chain polyunsaturated fatty acids into pork, as well as increasing the predicted lean yield of the carcass.

The micro-pathological characteristics in cerebral arteriovenous malformations(cAVMs).

Rupture and hemorrhage is the most serious complication of cerebral arteriovenous malformation(cAVMs), and have a significant impact on quality of life. We investigated the hematoxylin and eosin staining and ultrastructural features of cAVMs and characterized the abnormal vascular structure of cAVMs. Light and electron microscopy were performed on a series of pathological specimens obtained from 12 patients with cAVMs who underwent surgical resection for the first time without radiosurgery or embolization therapy. In tunica intima, we found that the vascular endothelial cells of cAVMs were damaged, and the lysis of the cell body occurred in multiple regions. In tunica media, the arrangement of the elastic layer was disordered, and the thickness was uneven. Part of the structure of the elastic lamina was missing. The part of tunica adventitia was fractured and discontinuous. In addition, we also observed the phenomenon that different blood vessels share the same vascular wall. Macrophage phagocytosis and lymphocyte infiltration in the adventitial region of ruptured cAVMs. Abnormal lipid deposition in vascular endothelial cells and smooth muscle cells. The structural incompleteness of cAVMs may be an important cause of hemorrhage.

Identification and characterization of circRNAs related to meat quality during embryonic development of the longissimus dorsi muscle in two pig breeds.

Meat quality, an important economic trait, is regulated by many factors, especially by genetic factors, including coding genes, miRNAs, and lncRNAs. Recent studies have elucidated that circRNAs also play a key role in muscle development and lipid deposition. However, the functions and regulatory mechanisms of circRNAs in meat quality remain mostly unknown. The circRNA expression profiles between Huainan pigs (Chinese indigenous pigs, fat-type, Huainan HN) and Large White pigs (Western commercial pigs, lean-type, LW) in the longissimus dorsi (LD) muscle at 38, 58, and 78days post conception (dpc) were compared by sequencing. In total, 39,887 circRNAs were identified in 18 samples, and 60, 78, and 86 differentially expressed circRNAs (DECs) were found at the three stages mentioned above between these two breeds. The parent genes of DECs were enriched in myogenesis, proliferation, adipogenesis and muscle fiber-type transition. The circRNA-miRNA interaction networks included 38 DECs and 47 miRNAs, and these miRNAs were involved in muscle development and lipid metabolism. Two shared DECs (circ_0030593 and circ_0032760) of these three stages were selected, their head-to-tail junction sites were validated by Sanger sequencing, and RT‒qPCR results suggested that these two DECs might be involved in intramuscular fat deposition. These findings provide a basis for understanding the role of circRNAs in meat quality.

The acromegaly lipodystrophy.

Growth hormone (GH) and insulin-like growth factor 1 (IGF-1) are essential to normal growth, metabolism, and body composition, but in acromegaly, excesses of these hormones strikingly alter them. In recent years, the use of modern methodologies to assess body composition in patients with acromegaly has revealed novel aspects of the acromegaly phenotype. In particular, acromegaly presents a unique pattern of body composition changes in the setting of insulin resistance that we propose herein to be considered an acromegaly-specific lipodystrophy. The lipodystrophy, initiated by a distinctive GH-driven adipose tissue dysregulation, features insulin resistance in the setting of reduced visceral adipose tissue (VAT) mass and intra-hepatic lipid (IHL) but with lipid redistribution, resulting in ectopic lipid deposition in muscle. With recovery of the lipodystrophy, adipose tissue mass, especially that of VAT and IHL, rises, but insulin resistance is lessened. Abnormalities of adipose tissue adipokines may play a role in the disordered adipose tissue metabolism and insulin resistance of the lipodystrophy. The orexigenic hormone ghrelin and peptide Agouti-related peptide may also be affected by active acromegaly as well as variably by acromegaly therapies, which may contribute to the lipodystrophy. Understanding the pathophysiology of the lipodystrophy and how acromegaly therapies differentially reverse its features may be important to optimizing the long-term outcome for patients with this disease. This perspective describes evidence in support of this acromegaly lipodystrophy model and its relevance to acromegaly pathophysiology and the treatment of patients with acromegaly.

Exploring the Preventive and Restorative Functions of Lactobacillus pentosus in Flesh Deterioration Caused by Oxidized Fish Oil Diets in Hybrid Grouper (♀ Epinephelus fuscoguttatus × ♂ E. lanceolatu)

The purpose was to investigate the preventive and restorative functions of Lactobacillus pentosus of hybrid grouper (♀ Epinephelus fuscoguttatus×♂ E. lanceolatu) flesh due to ingestion oxidized fish oil (OFO) diet. Basal diets were formulated using OFO as main lipid source and 1.0 × 10 9 CFU/g of L. pentosus was added to basal diet as experimental diet. Control group (OFO: 60 d basal diet), prevention group (OFOP: 30 d experimental diet + 30 d basal diet ), and restoration group (OFOR: 30 d basal diet + 30 d experimental diet ) were set up for grouper experiment with triplication. The results show that compared with the OFO group, the OFOP and OFOR groups significantly decreased muscle lipid deposition and lipid peroxidation production. The OFOP and OFOR groups significantly increased the polyunsaturated fatty acid content furthermore to improve nutritional value of muscle compared to the OFO group. Intervention with L. pentosus significantly influenced muscle flavor. OFOP and OFOR groups significantly upregulated expression of partial growth factor-related genes while downregulating expression of antioxidant-related genes. Consequently, the intervention of L. pentosus decreased lipid deposition and improved the nutritional value and flavor of grouper muscle, and it was recommended as a probiotic to prevent the deterioration of aquatic product quality.

Adipose Dysfunction in Adulthood Insulin Resistance of Low-Birth Weight Mice: A Proteomics Study.

PurposeTo investigate changes in the protein expression profile of white adipose tissue in low-birth weight (LBW) mice with high-fat diets using tandem mass tag (TMT) and liquid chromatography-mass spectrometry (LC-MS/MS) and parallel reaction monitoring (PRM).MethodsInstitute of Cancer Research (ICR) mice were used to establish an LBW model using malnutrition during pregnancy. Male pups were randomly selected from LBW and normal-birth weight (NBW) offspring, then all given a high-fat diet. Blood glucose, serum insulin, total cholesterol (TC) and triglyceride (TG) levels were measured. The weight ratio of liver, muscle, and adiposity index were calculated. Hematoxylin and eosin staining was used to visualize adipose tissue morphology. Oil red O staining of liver and TG content of muscle were used to determine ectopic lipid deposition. TMT combined with LC-MS/MS was used to analyze protein expression in white adipose tissue. PRM and Western blot were used to verify the expression of CD36, SCD1, PCK1 and PPARγ.ResultsCompared with NBW mice, fasting blood glucose, insulin and HOMA-IR significantly increased in LBW mice, indicating insulin resistance and impaired glucose regulation; TC, TG, adipocyte size, and adiposity index were increased in LBW mice, suggesting obesity and disorder of lipid metabolism. We observed ectopic lipid deposition in liver and muscle. There were 996 differentially expressed proteins (DEPs) in the LBW/NBW groups. Peroxisome proliferator-activated receptor (PPAR) was a relatively important signaling pathway regulating metabolic process in functional enrichment analysis of DEPs. Up-regulated expression of CD36, SCD1, and PCK1 in the adipose tissue of LBW mice was observed through PPAR pathways cluster analysis. And PRM and Western blot assay validated the proteomics findings.ConclusionWhen exposed to high-fat diets, LBW mice exhibited insulin resistance and disorder of lipid metabolism compared with NBW mice. The expression of PPARγ was elevated, as well as upstream CD36, downstream SCD1 and PCK1 of the PPARγ in the adipose tissue of LBW mice. It was suggested that the activation in CD36/PPARγ/SCD1 and CD36/PPARγ/PCK1 pathways may induce adipose dysfunction, thereby increasing susceptibility to insulin resistance.

A comparison of hepatic lipid metabolism and fatty acid composition in muscle between Duroc × Landrace × Yorkshire and Tibetan pigs from three regions

Qinghai-Tibet Plateau with an average altitude above 4000 m provides favorable conditions for Tibetan pigs that may have different meat quality from other pig breeds. This study was designed to compare the differences in lipid metabolism in liver and fatty acid composition in muscle between Tibetan and Duroc × Landrace × Yorkshire (DLY) pigs. Aba Tibetan pigs (n = 10), Gannan Tibetan pigs (n = 9), Nyingchi Tibetan pigs (n = 10) and DLY pigs (n = 10) were selected for the experiment. After fasting for 12 hours, they were slaughtered and blood, liver and muscle samples were taken for biochemical analyses. The results showed that the intramuscular fat content was not significantly different for Tibetan pigs among the three regions (<i>P</i> &gt; 0.05), which was significantly higher than that of DLY pigs (<i>P</i> &lt; 0.05). However, the liver fat content of Gannan Tibetan pigs was significantly lower than those of DLY pigs and Aba and Nyingchi Tibetan pigs (<i>P</i> &lt; 0.05). The hepatic lipid metabolism may be stronger in DLY pigs than in Tibetan pigs, but lipid deposition in muscle is weaker in DLY pigs than that in Tibetan pigs. Aba Tibetan pigs and Nyingchi Tibetan pigs had similar proportions of saturated, monounsaturated and polyunsaturated fatty acids, while Gannan Tibetan pigs and DLY pigs had similar types of fatty acids. The findings provide new insight into mechanisms of environmental and breed effects on the pork quality.

Comparative expression of genes implicated in lipid metabolism in different tissues of Barbari goats

The expression of genes linked to lipid metabolism mainly in lipogenesis, lipid transport and deposition contributes to the quality and composition of fat/lipids in the tissues. The present study investigated the expression changes in genes implicated in lipid biosynthesis (AGPAT2, DGAT2, FASN and GPAM), transport of fatty acids (FABP3) and lipid deposition (PLIN4) in muscles, liver, pancreas and kidney of Barbari goats. Real time quantitative PCR (polymerase chain reaction) analysis was used to estimate the expression level of different genes in the tissue samples. The expression of AGPAT2, DGAT2 and GPAM genes was higher in the liver while FASN was significantly (p<0.01) higher in skeletal muscles. FABP3 gene that coordinates transportation and signalling of lipids, as well as PLIN4 associated with fat deposition were mainly expressed in the muscles. The present study offers insight into the differential expression of genes involved in lipid metabolism in different tissues of Barbari goat.

Impacts of Betaine Addition in Sow and Piglet's Diets on Growth Performance, Plasma Hormone, and Lipid Metabolism of Bama Mini-Pigs.

The present study evaluated the effects of betaine addition in sow and piglet's diets on growth performance, plasma hormone, and lipid metabolism of Bama mini-pigs. A total of 26 pregnant Bama mini-pigs and 104 weaned piglets were selected and divided into different dietary treatment groups (details in “Materials and Methods”). Blood and muscle samples were collected at 65-, 95-, and 125-day-old, respectively. The results showed that betaine addition in sow-offspring diets increased (P < 0.05) the body weight at 125-day-old, average daily gain from 35- to 65-day-old, and average daily feed intake at 35–65 and 35–95 days old of pigs compared with the control group. Betaine addition in sow-offspring diets increased (P < 0.05) the plasma gastrin level at 95-day-old, while betaine addition in sow diets decreased (P < 0.05) the plasma peptide YY and leptin levels at 65-day-old pigs. In the longissimus dorsi muscle of pigs, betaine addition in sow and sow-offspring diets increased (P < 0.05) the C12:0 content at 65-day-old while decreased at 95-day-old. Moreover, betaine addition in sow-offspring diets increased the C24:0 content and decreased the C18:1n9t content at 125-day-old (P < 0.05). In the biceps femoris muscle, the contents of C12:0 at 65-day-old and C20:4n6 at 125-day-old were decreased (P < 0.05) after the betaine addition in both sow and piglet's diets. In addition, betaine addition in sow diets decreased (P < 0.05) the C20:0 content at 125-day-old, while betaine addition in sow-offspring diets increased the C18:3n6 and decreased C24:0 contents at 65-day-old pigs (P < 0.05). In the psoas major muscle, betaine addition in sow and sow-offspring diets decreased (P < 0.05) the contents of C18:1n9t at 65-day-old and C20:1 at 95-day-old, while betaine addition in sow diets decreased (P < 0.05) the intramuscular fat content at 125-day-old. Moreover, betaine addition in sow-offspring diets was also associated with muscle lipid deposition and metabolisms by regulating the gene expressions related to fatty acid metabolism. These findings suggested that betaine addition in sow-offspring diets could improve the growth performance, whereas betaine addition in both sow and sow-offspring diets could enhance lipid quality by altering plasma hormone level and fatty acid composition and regulating the gene expressions related to fatty acid metabolism.