Angiopoietin-like protein 4 regulates breast muscle lipid metabolism in broilers

Iodothyronines such as triiodothyronine (T3) and 3,5-diiodothyronine (T2) influence energy expenditure and lipid metabolism. Skeletal muscle contributes significantly to energy homeostasis, and the above iodothyronines are known to act on this tissue. However, little is known about the cellular/molecular events underlying the effects of T3 and T2 on skeletal muscle lipid handling. Since FAT/CD36 is involved in the utilization of free fatty acids by skeletal muscle, specifically in their import into that tissue and presumably their oxidation at the mitochondrial level, we hypothesized that related changes in lipid handling and in FAT/CD36 expression and subcellular redistribution would occur due to hypothyroidism and to T3 or T2 administration to hypothyroid rats. In gastrocnemius muscles isolated from hypothyroid rats, FAT/CD36 was upregulated (mRNA levels and total tissue, sarcolemmal, and mitochondrial protein levels). Administration of either T3 or T2 to hypothyroid rats resulted in 1) little or no change in FAT/CD36 mRNA level, 2) a decreased total FAT/CD36 protein level, and 3) further increases in FAT/CD36 protein level in sarcolemma and mitochondria. Thus, the main effect of each iodothyronine seemed to be exerted at the level of FAT/CD36 cellular distribution. The effect of further increases in FAT/CD36 protein level in sarcolemma and mitochondria was already evident at 1 h after iodothyronine administration. Each iodothyronine increased the mitochondrial fatty acid oxidation rate. However, the mechanisms underlying their rapid effects seem to differ; T2 and T3 each induce FAT/CD36 translocation to mitochondria, but only T2 induces increases in carnitine palmitoyl transferase system activity and in the mitochondrial substrate oxidation rate.

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Effects of epinephrine on lipid metabolism in resting skeletal muscle

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1998.275.2.e300 ◽

1998 ◽

Vol 275 (2) ◽

pp. E300-E309 ◽

Cited By ~ 27

Author(s):

Sandra J. Peters ◽

David J. Dyck ◽

Arend Bonen ◽

Lawrence L. Spriet

Keyword(s):

Skeletal Muscle ◽

Lipid Metabolism ◽

Lipid Synthesis ◽

Hormone Sensitive Lipase ◽

Simultaneous Estimation ◽

Lipid Hydrolysis ◽

Muscle Lipid ◽

Triacylglycerol Hydrolysis ◽

Skeletal Muscle Lipid ◽

Glycogen Breakdown

The effects of physiological (0, 0.1, 2.5, and 10 nM) and pharmacological (200 nM) epinephrine concentrations on resting skeletal muscle lipid metabolism were investigated with the use of incubated rat epitrochlearis (EPT), flexor digitorum brevis (FDB), and soleus (SOL) muscles. Muscles were chosen to reflect a range of oxidative capacities: SOL > EPT > FDB. The muscles were pulsed with [1-14C]palmitate and chased with [9,10-3H]palmitate. Incorporation and loss of the labeled palmitate from the triacylglycerol pool (as well as mono- and diacylglycerol, phospholipid, and fatty acid pools) permitted the simultaneous estimation of lipid hydrolysis and synthesis. Endogenous and exogenous fat oxidation was quantified by14CO2and3H2O production, respectively. Triacylglycerol breakdown was elevated above control at all epinephrine concentrations in the oxidative SOL muscle, at 2.5 and 200 nM (at 10 nM, P= 0.066) in the FDB, and only at 200 nM epinephrine in the EPT. Epinephrine stimulated glycogen breakdown in the EPT at all concentrations but only at 10 and 200 nM in the FDB and had no effect in the SOL. We further characterized muscle lipid hydrolysis potential and measured total hormone-sensitive lipase content by Western blotting (SOL > FDB > EPT). This study demonstrated that physiological levels of epinephrine cause measurable increases in triacylglycerol hydrolysis at rest in oxidative but not in glycolytic muscle, with no change in the rate of lipid synthesis or oxidation. Furthermore, epinephrine caused differential stimulation of carbohydrate and fat metabolism in glycolytic vs. oxidative muscle. Epinephrine preferentially stimulated glycogen breakdown over triacylglycerol hydrolysis in the glycolytic EPT muscle. Conversely, in the oxidative SOL muscle, epinephrine caused an increase in endogenous lipid hydrolysis over glycogen breakdown.

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Muscle Lipid Metabolism and Insulin Secretion Are Altered in Insulin-Resistant Rats Fed a High Sucrose Diet

Journal of Nutrition ◽

10.1093/jn/133.1.127 ◽

2003 ◽

Vol 133 (1) ◽

pp. 127-133 ◽

Cited By ~ 68

Author(s):

Adriana Chicco ◽

María Eugenia D'Alessandro ◽

Liliana Karabatas ◽

Claudia Pastorale ◽

Juan Carlos Basabe ◽

...

Keyword(s):

Insulin Secretion ◽

Lipid Metabolism ◽

Muscle Lipid ◽

Insulin Resistant ◽

Sucrose Diet ◽

High Sucrose Diet ◽

High Sucrose

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Role of proton MR for the study of muscle lipid metabolism

NMR in Biomedicine ◽

10.1002/nbm.1096 ◽

2006 ◽

Vol 19 (7) ◽

pp. 968-988 ◽

Cited By ~ 138

Author(s):

Chris Boesch ◽

Juergen Machann ◽

Peter Vermathen ◽

Fritz Schick

Keyword(s):

Lipid Metabolism ◽

Muscle Lipid

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Transcriptional insights into key genes and pathways controlling muscle lipid metabolism in broiler chickens

BMC Genomics ◽

10.1186/s12864-019-6221-0 ◽

2019 ◽

Vol 20 (1) ◽

Cited By ~ 2

Author(s):

Lu Liu ◽

Xiaojing Liu ◽

Huanxian Cui ◽

Ranran Liu ◽

Guiping Zhao ◽

...

Keyword(s):

Lipid Metabolism ◽

Muscle Tissue ◽

Broiler Chickens ◽

Lipid Deposition ◽

Pectoralis Muscle ◽

Steroid Biosynthesis ◽

Muscle Lipid ◽

Ppar Signaling ◽

Key Genes ◽

Key Pathways

Abstract Background Intramuscular fat (IMF) is one of the most important factors positively associated with meat quality. Triglycerides (TGs), as the main component of IMF, play an essential role in muscle lipid metabolism. This transcriptome analysis of pectoralis muscle tissue aimed to identify functional genes and biological pathways likely contributing to the extreme differences in the TG content of broiler chickens. Results The study included Jingxing-Huang broilers that were significantly different in TG content (5.81 mg/g and 2.26 mg/g, p < 0.01) and deposition of cholesterol also showed the same trend. This RNA sequencing analysis was performed on pectoralis muscle samples from the higher TG content group (HTG) and the lower TG content group (LTG) chickens. A total of 1200 differentially expressed genes (DEGs) were identified between two groups, of which 59 DEGs were related to TG and steroid metabolism. The HTG chickens overexpressed numerous genes related to adipogenesis and lipogenesis in pectoralis muscle tissue, including the key genes ADIPOQ, CD36, FABP4, FABP5, LPL, SCD, PLIN1, CIDEC and PPARG, as well as genes related to steroid biosynthesis (DHCR24, LSS, MSMO1, NSDHL and CH25H). Additionally, key pathways related to lipid storage and metabolism (the steroid biosynthesis and peroxisome proliferator activated receptor (PPAR) signaling pathway) may be the key pathways regulating differential lipid deposition between HTG group and LTG group. Conclusions This study showed that increased TG deposition accompanying an increase in steroid synthesis in pectoralis muscle tissue. Our findings of changes in gene expression of steroid biosynthesis and PPAR signaling pathway in HTG and LTG chickens provide insight into genetic mechanisms involved in different lipid deposition patterns in pectoralis muscle tissue.

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Development of leptin resistance in rat soleus muscle in response to high-fat diets

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.2000.279.6.e1374 ◽

2000 ◽

Vol 279 (6) ◽

pp. E1374-E1382 ◽

Cited By ~ 81

Author(s):

Greg R. Steinberg ◽

David J. Dyck

Keyword(s):

Skeletal Muscle ◽

Lipid Metabolism ◽

Soleus Muscle ◽

Leptin Resistance ◽

Safflower Oil ◽

High Fat ◽

Muscle Lipid ◽

High Fat Diets ◽

Rat Soleus Muscle ◽

Fat Diets

Direct evidence for leptin resistance in peripheral tissues such as skeletal muscle does not exist. Therefore, we investigated the effects of different high-fat diets on lipid metabolism in isolated rat soleus muscle and specifically explored whether leptin's stimulatory effects on muscle lipid metabolism would be reduced after exposure to high-fat diets. Control (Cont, 12% kcal fat) and high-fat [60% kcal safflower oil (n-6) (HF-Saff); 48% kcal safflower oil plus 12% fish oil (n-3)] diets were fed to rats for 4 wk. After the dietary treatments, muscle lipid turnover and oxidation in the presence and absence of leptin was measured using pulse-chase procedures in incubated resting soleus muscle. In the absence of leptin, phospholipid, diacylglycerol, and triacylglycerol (TG) turnover were unaffected by the high-fat diets, but exogenous palmitate oxidation was significantly increased in the HF-Saff group. In Cont rats, leptin increased exogenous palmitate oxidation (21.4 ± 5.7 vs. 11.9 ± 1.61 nmol/g, P = 0.019) and TG breakdown (39.8 ± 5.6 vs. 27.0 ± 5.2 nmol/g, P = 0.043) and decreased TG esterification (132.5 ± 14.6 vs. 177.7 ± 29.6 nmol/g, P = 0.043). However, in both high-fat groups, the stimulatory effect of leptin on muscle lipid oxidation and hydrolysis was eliminated. Partial substitution of fish oil resulted only in the restoration of leptin's inhibition of TG esterification. Thus we hypothesize that, during the development of obesity, skeletal muscle becomes resistant to the effects of leptin, resulting in the accumulation of intramuscular TG. This may be an important initiating step in the development of insulin resistance common in obesity.

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