scholarly journals The effect of short-term fasting on liver and skeletal muscle lipid, glucose, and energy metabolism in healthy women and men

2011 ◽  
Vol 53 (3) ◽  
pp. 577-586 ◽  
Author(s):  
Jeffrey D. Browning ◽  
Jeannie Baxter ◽  
Santhosh Satapati ◽  
Shawn C. Burgess
Keyword(s):  
Skeletal Muscle ◽  
Energy Metabolism ◽  
Short Term ◽  
Muscle Lipid ◽  
Healthy Women ◽  
Skeletal Muscle Lipid

Short-term fasting increases skeletal muscle lipid content in association with enhanced mRNA levels of lipoprotein lipase 1 in lean juvenile red seabream ( Pagrus major )

Aquaculture ◽  
2016 ◽  
Vol 452 ◽  
pp. 160-168 ◽  
Author(s):  
Gen Kaneko ◽  
Hirohito Shirakami ◽  
Toshihiro Yamada ◽  
Shin-ichiro Ide ◽  
Yutaka Haga ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lipoprotein Lipase ◽  
Lipid Content ◽  
Mrna Levels ◽  
Pagrus Major ◽  
Short Term ◽  
Muscle Lipid ◽  
Red Seabream ◽  
Skeletal Muscle Lipid

scholarly journals Effects of short‐term exercise combined with either high or low glycemic diets on skeletal muscle lipid content in older, insulin resistant adults

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Jacob M Haus ◽  
Kelly K Covey ◽  
John A Jessberger ◽  
Latina M Brooks ◽  
Sangeeta R Kashyap ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lipid Content ◽  
Short Term ◽  
Muscle Lipid ◽  
Insulin Resistant ◽  
Skeletal Muscle Lipid

Intramyocellular fat storage in metabolic diseases

2016 ◽  
Vol 26 (1) ◽  
Author(s):  
Claire Laurens ◽  
Cedric Moro
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Metabolic Diseases ◽  
Recent Literature ◽  
Lipid Storage ◽  
Muscle Lipid ◽  
The Past ◽  
Skeletal Muscle Lipid ◽  
Ectopic Lipid Storage

AbstractOver the past decades, obesity and its metabolic co-morbidities such as type 2 diabetes (T2D) developed to reach an endemic scale. However, the mechanisms leading to the development of T2D are still poorly understood. One main predictor for T2D seems to be lipid accumulation in “non-adipose” tissues, best known as ectopic lipid storage. A growing body of data suggests that these lipids may play a role in impairing insulin action in metabolic tissues, such as liver and skeletal muscle. This review aims to discuss recent literature linking ectopic lipid storage and insulin resistance, with emphasis on lipid deposition in skeletal muscle. The link between skeletal muscle lipid content and insulin sensitivity, as well as the mechanisms of lipid-induced insulin resistance and potential therapeutic strategies to alleviate lipotoxic lipid pressure in skeletal muscle will be discussed.

Responses of skeletal muscle lipid metabolism in rat gastrocnemius to hypothyroidism and iodothyronine administration: a putative role for FAT/CD36

2012 ◽  
Vol 303 (10) ◽  
pp. E1222-E1233 ◽  
Author(s):  
Assunta Lombardi ◽  
Rita De Matteis ◽  
Maria Moreno ◽  
Laura Napolitano ◽  
Rosa Anna Busiello ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lipid Metabolism ◽  
Protein Level ◽  
Oxidation Rate ◽  
Mitochondrial Protein ◽  
Acid Oxidation ◽  
Mrna Levels ◽  
Muscle Lipid ◽  
Mitochondrial Fatty Acid ◽  
Skeletal Muscle Lipid

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.

scholarly journals Effects of epinephrine on lipid metabolism in resting skeletal muscle

1998 ◽  
Vol 275 (2) ◽  
pp. E300-E309 ◽  
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.

Proteome of Skeletal Muscle Lipid Droplet Reveals Association with Mitochondria and Apolipoprotein A-I

2011 ◽  
Vol 10 (10) ◽  
pp. 4757-4768 ◽  
Author(s):  
Huina Zhang ◽  
Yang Wang ◽  
Jing Li ◽  
Jinhai Yu ◽  
Jing Pu ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lipid Droplet ◽  
Muscle Lipid ◽  
Apolipoprotein A ◽  
Skeletal Muscle Lipid

Age-related differences in skeletal muscle lipid profiles of Weddell seals: clues to developmental changes

2010 ◽  
Vol 213 (10) ◽  
pp. 1676-1684 ◽  
Author(s):  
S. J. Trumble ◽  
S. R. Noren ◽  
L. A. Cornick ◽  
T. J. Hawke ◽  
S. B. Kanatous
Keyword(s):  
Skeletal Muscle ◽  
Lipid Profiles ◽  
Developmental Changes ◽  
Muscle Lipid ◽  
Weddell Seals ◽  
Age Related ◽  
Skeletal Muscle Lipid
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