MJ Watt, EW Kraegen - Diabetes, 2009 - Am Diabetes Assoc The evidence is now compelling that an excess supply of fatty acids, beyond that
required for energy needs, is a cause of muscle insulin resistance.
Intramyocellular triglyceride accumulation is a marker of excess fatty acid ... Cited by 1 - Related articles - All 3 versions
AST Bickerton, R Roberts, BA Fielding, H … - Diabetologia, 2008 - Springer Abstract Aims/hypothesis Increased NEFA production and concen- trations may
underlie insulin resistance. We examined systemic and adipose tissue NEFA
metabolism in insulin- resistant overweight men (BMI 25–35 kg/m2). ... Cited by 8 - Related articles - All 3 versions
K Won Park, DS Halperin, P Tontonoz - Cell Metabolism, 2008 - Elsevier Adipocytes are central to the control of energy balance and lipid homeostasis.
The ability to store excess energy in adipose tissue is an important
evolutionary adaptation. However, obesity, the excess accumulation of ... Cited by 4 - Related articles - All 4 versions
L Makowski, RC Noland, TR Koves, W Xing, … - The FASEB Journal, 2009 - FASEB Peroxisome proliferator-activated receptor- (PPAR ) is a master transcriptional
regulator of β-oxidation and a prominent target of hypolipidemic drugs. To gain
deeper insights into the systemic consequences of impaired fat catabolism, ... Cited by 4 - Related articles - All 4 versions
T Cadoudal, E Distel, S Durant, F Fouque, JM … - Diabetes, 2008 - Am Diabetes Assoc RESULTS—Rosiglitazone increased PDK4 mRNA in all WAT depots but not in liver
and muscle. PDK2 transcript was not affected. This isoform selectivity was also
found in ex vivo–treated explants. In 3T3-F442A adipocytes, Pdk4 ... Cited by 6 - Related articles - All 4 versions
- ►jbc.org CW Lu, SC Lin, KF Chen, YY Lai, SJ Tsai - Journal of Biological Chemistry, 2008 - ASBMB The switch of cellular metabolism from mitochondrial respiration to glycolysis
is the hallmark of cancer cells and associated with tumor malignancy. However,
the mechanism of this metabolic switch remains largely unknown. Herein, we ... Cited by 7 - Related articles - All 3 versions
- ►cardiovascres.org X Palomer, D Alvarez-Guardia, R Rodriguez- … - Cardiovascular Research, 2009 - cardiovascres.org Methods and results: Exposure of AC16 cells to TNF- inhibited the expression of
peroxisome proliferator-activated receptor coactivator 1 (PGC-1 ), an upstream
regulator of lipid and glucose oxidative metabolism. Studies performed with ... Cited by 5 - Related articles - All 4 versions
- ►diabetesjournals.org CR Bruce, AJ Hoy, N Turner, MJ Watt, TL … - Diabetes, 2009 - Am Diabetes Assoc OBJECTIVE—Skeletal muscle insulin resistance is associated with lipid
accumulation, but whether insulin resistance is due to reduced or enhanced flux
of long-chain fatty acids into the mitochondria is both controversial and ... Cited by 7 - Related articles - All 3 versions
H Wang, LA Knaub, DR Jensen, D Young Jung … - Diabetes, 2009 - Am Diabetes Assoc RESULTS—Nine-week-old SMLPL −/− mice showed no differences in body weight,
fat mass, or whole-body insulin sensitivity, but older SMLPL −/− mice had
greater weight gain and whole-body insulin resistance. High-fat diet ... Cited by 13 - Related articles - All 5 versions
C Gaudel, PA Grimaldi - PPAR research, 2007 - hindawi.com Peroxisome proliferator-activated receptors (PPARs) are transcription factors
that act as lipid sensors and adapt the metabolic rates of various tissues to
the concentration of dietary lipids. PPARs are pharmacological targets for ... Cited by 7 - Related articles - View as HTML - All 7 versions
