Assessment of Intrahepatic Triglyceride Content Using Magnetic Resonance Spectroscopy

Frimel, Tiffany N.; Deivanayagam, Sheela; Bashir, Adil; O’Connor, Robert; Klein, Samuel

doi:10.1111/j.1559-4564.2007.07168.x

Cited by 40 publications

(35 citation statements)

References 21 publications

(33 reference statements)

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“…Images of a sagittal, coronal, and axial cube of 2 cm 3 volume in the right lobe of the liver were acquired. Quantification of the spectra (water and methylene resonances) was performed as described previously [19,26]. Areas of resonance from water protons and methylene groups in fatty acid chains were obtained with a time-domain nonlinear fitting routine using commercial software (Syngo spectroscopy VB15, Siemens).…”

Section: Measurement Of Intrahepatic Triglyceride Content and Abdominmentioning

confidence: 99%

Intrahepatic triglyceride content is independently associated with chronic kidney disease in obese adults: A cross-sectional study

et al. 2015

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Section: Measurement Of Intrahepatic Triglyceride Content and Abdominmentioning

confidence: 99%

Intrahepatic triglyceride content is independently associated with chronic kidney disease in obese adults: A cross-sectional study

et al. 2015

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“…Body fat mass (FM) and fat-free mass (FFM) were determined by using dual-energy x-ray absorptiometry (Delphi-W densitometer, Hologic). Intraabdominal and abdominal s.c. adipose tissue volumes were quantified by magnetic resonance imaging (Siemens; ANALYZE 7.0 software, Mayo Foundation) (9) and IHTG content was measured by using proton magnetic resonance spectroscopy (Siemens) as we have previously described (42).…”

Section: Methodsmentioning

confidence: 99%

Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity

Fabbrini

Magkos

Mohammed

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Visceral adipose tissue (VAT) is an important risk factor for obesityrelated metabolic disorders. Therefore, a reduction in VAT has become a key goal in obesity management. However, VAT is correlated with intrahepatic triglyceride (IHTG) content, so it is possible that IHTG, not VAT, is a better marker of metabolic disease. We determined the independent association of IHTG and VAT to metabolic function, by evaluating groups of obese subjects, who differed in IHTG content (high or normal) but matched on VAT volume or differed in VAT volume (high or low) but matched on IHTG content. Stable isotope tracer techniques and the euglycemic-hyperinsulinemic clamp procedure were used to assess insulin sensitivity and very-lowdensity lipoprotein-triglyceride (VLDL-TG) secretion rate. Tissue biopsies were obtained to evaluate cellular factors involved in ectopic triglyceride accumulation. Hepatic, adipose tissue and muscle insulin sensitivity were 41, 13, and 36% lower (P < 0.01), whereas VLDLtriglyceride secretion rate was almost double (P < 0.001), in subjects with higher than normal IHTG content, matched on VAT. No differences in insulin sensitivity or VLDL-TG secretion were observed between subjects with different VAT volumes, matched on IHTG content. Adipose tissue CD36 expression was lower (P < 0.05), whereas skeletal muscle CD36 expression was higher (P < 0.05), in subjects with higher than normal IHTG. These data demonstrate that IHTG, not VAT, is a better marker of the metabolic derangements associated with obesity. Furthermore, alterations in tissue fatty acid transport could be involved in the pathogenesis of ectopic triglyceride accumulation by redirecting plasma fatty acid uptake from adipose tissue toward other tissues.abdominal fat ͉ insulin resistance ͉ NAFLD ͉ steatosis ͉ VLDL V isceral adipose tissue (VAT) is an important and independent predictor of metabolic risk factors for coronary heart disease, particularly diabetes and dyslipidemia (1, 2). Moreover, data from metabolic studies conducted on human subjects (3, 4) indicate that an increase in VAT is associated with impaired glucose tolerance, insulin resistance, and increased very-low-density lipoproteintriglyceride (VLDL-TG) secretion. These observations and the unique anatomical location of visceral fat, which releases free fatty acids (FFA) and adipokines into the portal vein for direct transport to the liver, have led to the concept that VAT is responsible for many of the metabolic abnormalities associated with abdominal obesity (5, 6). Therefore, a reduction in visceral fat has become a key therapeutic goal in the management of obesity (6, 7).Although VAT is associated with metabolic disease, a causal link between VAT and metabolic dysfunction has not been demonstrated in humans. Recently, it has become clear that VAT correlates directly with intrahepatic triglyceride (IHTG) content (8-10), and an increase in IHTG is associated with the same metabolic abnormalities linked to an increase in VAT (9-12). Therefore, it is possible that VAT itself is n...

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“…Body FM and FFM were determined using dualenergy x-ray absorptiometry (Lunar iDXA; GE Healthcare). VAT and s.c. abdominal adipose tissue volumes were quantified using MRI (Siemens; Analyze 7.0 software; Mayo Clinic, Mayo Foundation), and IHTG content was determined using magnetic resonance spectroscopy (Siemens) (38).…”

Section: Methodsmentioning

confidence: 99%

Metabolically normal obese people are protected from adverse effects following weight gain

Fabbrini¹,

Yoshino²,

Yoshino³

et al. 2015

J. Clin. Invest.

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BACKGROUND.Obesity is associated with insulin resistance and increased intrahepatic triglyceride (IHTG) content, both of which are key risk factors for diabetes and cardiovascular disease. However, a subset of obese people does not develop these metabolic complications. Here, we tested the hypothesis that people defined by IHTG content and insulin sensitivity as "metabolically normal obese" (MNO), but not those defined as "metabolically abnormal obese" (MAO), are protected from the adverse metabolic effects of weight gain. METHODS.Body composition, multiorgan insulin sensitivity, VLDL apolipoprotein B100 (apoB100) kinetics, and global transcriptional profile in adipose tissue were evaluated before and after moderate (~6%) weight gain in MNO (n = 12) and MAO (n = 8) subjects with a mean BMI of 36 ± 4 kg/m 2 who were matched for BMI and fat mass. RESULTS.Although the increase in body weight and fat mass was the same in both groups, hepatic, skeletal muscle, and adipose tissue insulin sensitivity deteriorated, and VLDL apoB100 concentrations and secretion rates increased in MAO, but not MNO, subjects. Moreover, biological pathways and genes associated with adipose tissue lipogenesis increased in MNO, but not MAO, subjects.CONCLUSIONS. These data demonstrate that MNO people are resistant, whereas MAO people are predisposed, to the adverse metabolic effects of moderate weight gain and that increased adipose tissue capacity for lipogenesis might help protect MNO people from weight gain-induced metabolic dysfunction.TRIAL REGISTRATION. ClinicalTrials.gov NCT01184170.

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Assessment of Intrahepatic Triglyceride Content Using Magnetic Resonance Spectroscopy

Cited by 40 publications

References 21 publications

Intrahepatic triglyceride content is independently associated with chronic kidney disease in obese adults: A cross-sectional study

Intrahepatic triglyceride content is independently associated with chronic kidney disease in obese adults: A cross-sectional study

Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity

Metabolically normal obese people are protected from adverse effects following weight gain

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