Intramyocellular Lipid and Insulin Resistance

Kuhlmann, Johanna; Neumann-Haefelin, Claudia; Belz, Ulrich; Kalisch, Jürgen; Juretschke, Hans-Paul; Stein, Marion; Kleinschmidt, Elke; Kramer, Werner; Herling, Andreas W.

doi:10.2337/diabetes.52.1.138

Cited by 124 publications

(99 citation statements)

References 52 publications

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“…These two parameters were measured using a volume selective spectroscopic method (VSEL, Bruker); IMCL at 7 Tesla and HepCl at 4.7 Tesla as described previously. 28 IMCL was detected in the TIB using a slotted resonator for rf-excitation and an actively decoupled surface coil for signal detection (voxel size 1.6 Â 1.6 Â 3.2 mm 3 ) and expressed as IMCL-to-tCr ratio. HepCl was detected in a homogeneous region of the liver (4 mm 3 ) using a resonator for rf transmit and receive and expressed as fatto-water ratio.…”

Section: Experimental Designmentioning

confidence: 99%

Reversal of visceral adiposity in candy-diet fed female Wistar rats by the CB1 receptor antagonist rimonabant

et al. 2008

Int J Obes

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Objective: The severity of obesity is often more determined by the distribution of fat depots rather than by body weight itself. Therefore, the effect of rimonabant on fat distribution pattern was investigated in female candy-fed Wistar rats. Design: Female Wistar rats were fed a high fat, high carbohydrate (candy-) diet for 12 weeks. During the last 6 weeks rats were treated with rimonabant. Food intake and body weight development were investigated, as well as effects on total body fat, especially visceral fat and ectopic lipid accumulation in skeletal muscle and liver, determined by in vivo magnetic resonance imaging/magnetic resonance spectroscopy. Results: Candy-diet increased body weight, which was predominantly due to the increased total fat mass with predominance of visceral fat accumulation. Treatment with rimonabant fully reversed the weight gain and fat deposition in the visceral cavity and skeletal muscle, in contrast to pair feeding. In spite of an only transient reduction of food intake, body weight reduction, as well as normalized body fat, reduced visceral fat and intramyocellular lipids were maintained over the treatment period. Conclusions: We conclude that additional factors other than reduced caloric intake must be responsible for the improvements in these lipid parameters. The complete cluster of results is consistent with increased lipid oxidation caused by rimonabant.

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Section: Experimental Designmentioning

confidence: 99%

Reversal of visceral adiposity in candy-diet fed female Wistar rats by the CB1 receptor antagonist rimonabant

et al. 2008

Int J Obes

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“…To investigate the influence of starvation on insulin sensitivity, euglycemic-hyperinsulinemic glucose clamp studies were performed on three groups of rats (n ϭ 7): 1) 12 h (reverse light-dark cycle), 2) 24 h, and 3) 72 h of starvation. The study was performed in anesthetized animals as described previously (28). Briefly, the study design consisted of a 120-min basal period followed by a 2-h euglycemichyperinsulinemic clamp.…”

Section: Methodsmentioning

confidence: 99%

“…MRS. In vivo MRS studies in anesthetized rats were performed on a 7-Tesla Biospec system (Bruker BioSpin, Ettlingen, Germany) as described previously (28). Briefly, IMCLs and HepCLs were observed using a single-voxel spectroscopy sequence.…”

Section: Methodsmentioning

confidence: 99%

Muscle-Type Specific Intramyocellular and Hepatic Lipid Metabolism During Starvation in Wistar Rats

Neumann-Haefelin

Beha²,

Kuhlmann³

et al. 2004

Diabetes

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“…With appropriate high-field MR systems (7 T or above), this measurement allows quantification of HTG in mice (19) and in the Zucker diabetic fatty (ZDF) rat model of T2DM (20) and is well suited for longitudinal measurements of HTGs in a single animal.…”

Section: Introductionmentioning

confidence: 99%

Sources of hepatic triglyceride accumulation during high‐fat feeding in the healthy rat

et al. 2008

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Hepatic triglyceride (HTG) accumulation from peripheral dietary sources and from endogenous de novo lipogenesis (DNL) was quantified in adult Sprague-Dawley rats by combining in vivo localized 1 H MRS measurement of total hepatic lipid with a novel ex vivo 2 H NMR analysis of HTG 2 H enrichment from 2 H-enriched body water. The methodology for DNL determination needs further validation against standard methodologies. To examine the effect of a high-fat diet on HTG concentrations and sources, animals (n ¼ 5) were given high-fat chow for 35 days. HTG accumulation, measured by in vivo 1 H MRS, increased significantly after 1 week (3.85 W 0.60% vs 2.13 W 0.34% for animals fed on a standard chow diet, P < 0.05) and was maintained until week 5 (3.30 W 0.60% vs 1.12 W 0.30%, P < 0.05). Animals fed on a high-fat diet were glucose intolerant (13.3 W 1.3 vs 9.4 W 0.8 mM in animals fed on a standard chow diet, for 60 min glycemia after glucose challenge, P < 0.05). In control animals, DNL accounted for 10.9 W 1.0% of HTG, whereas in animals given the high-fat diet, the DNL contribution was significantly reduced to 1.0 W 0.2% (P < 0.01 relative to controls). In a separate study to determine the response of HTG to weaning from a high-fat diet, animals with raised HTG (3.33 W 0.51%) after 7days of a high-fat diet reverted to basal HTG concentrations (0.76 W 0.06%) after an additional 7 days of weaning on a standard chow diet. These studies show that, in healthy rats, HTG concentrations are acutely influenced by dietary lipid concentrations. Although the DNL contribution to HTG content is suppressed by a high-fat diet in adult Sprague-Dawley rats, this effect is insufficient to prevent overall increases in HTG concentrations.

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Intramyocellular Lipid and Insulin Resistance

Cited by 124 publications

References 52 publications

Reversal of visceral adiposity in candy-diet fed female Wistar rats by the CB1 receptor antagonist rimonabant

Reversal of visceral adiposity in candy-diet fed female Wistar rats by the CB1 receptor antagonist rimonabant

Muscle-Type Specific Intramyocellular and Hepatic Lipid Metabolism During Starvation in Wistar Rats

Sources of hepatic triglyceride accumulation during high‐fat feeding in the healthy rat

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