Body composition analysis of obesity and hepatic steatosis in mice by relaxation compensated fat fraction (RCFF) MRI

Johnson, David H.; Narayan, Sreenath; Wilson, David L.; Flask, Chris A.

doi:10.1002/jmri.23508

Cited by 14 publications

(18 citation statements)

References 25 publications

(30 reference statements)

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“…5C(a)). Staining with PCNA demonstrated increased proliferative index of the glandular epithelium of the B6.V-Lepob/J mice, compared to C57BL/6N mice (23.26 AE 7.43 vs. 19.58 AE 5.52; P < 0.05], which might also contribute in increased prostate size ( Fig. 5C(b)).…”

Section: Resultsmentioning

confidence: 99%

Obesity‐initiated metabolic syndrome promotes urinary voiding dysfunction in a mouse model

Babcook

Shukla

et al. 2016

The Prostate

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OBJECTIVE Accumulating evidences suggests that obesity and metabolic syndrome (MetS) contribute towards lower urinary tract symptoms (LUTS) through alterations in the phenotype of bladder and prostate gland. Clinical studies indicate a link between MetS and LUTS. Nevertheless, there is lack of suitable animal model(s) which could illustrate an association linking obesity to LUTS. We examined the lower urinary tract function in an obesity-initiated MetS mouse model. METHODS Male C57BL/6N wild-type and obese B6.V-Lepob/J maintained on regular diet for 28 weeks were subjected to the assessment of body weight (BW), body length (BL), waist circumference (WC), body mass index (BMI), blood glucose (BG), plasma insulin (INS), plasma leptin (LEP), total cholesterol (CHO), free fatty acid (FFA) and measurement of urinary functions. Whole animal peritoneal and subcutaneous adipose tissue measurements as well as prostate and bladder volumes were analyzed by MRI followed by histological evaluation. These parameters were used to draw correlations between MetS and LUTS. RESULTS Obesity parameters such as BW, WC, and BMI were significantly higher in B6.V-Lepob/J mice compared to C57BL/6N mice (p<0.01). Higher levels of total CHO and FFA were noted in B6.V-Lepob/J mice than C57BL/6N mice (p<0.05). These results were concurrent with frequency, lower average urine volume and other urinary voiding dysfunctions in B6.V-Lepob/J mice. MRI assessments demonstrate marked increase in body fat and prostate volume in these mice. Compared to C57BL/6N mice, histological analysis of the prostate from B6.V-Lepob/J mice showed increased proliferation, gland crowding and infiltration of immune cells in the stroma; whereas the bladder urothelium was slightly thicker and appears more proliferative in these mice. The regression and correlation analysis indicate that peritoneal fat (R=0.853; p<0.02), CHO (R=0.729; p<0.001), BG (R=0.712; p<0.001) and prostate volume (R=0.706; p<0.023) strongly correlate with LUTS whereas BMI, WC, INS, and FFA moderately correlate with the prevalence of bladder dysfunction. CONCLUSION Our results suggest that LUTS may be attributable in part to obesity and MetS. Validation of an in vivo model may lead to understand the underlying pathophysiological mechanisms of obesity-related LUTS in humans.

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Section: Resultsmentioning

confidence: 99%

Obesity‐initiated metabolic syndrome promotes urinary voiding dysfunction in a mouse model

Babcook

Shukla

et al. 2016

The Prostate

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“…A 72-mm diameter volume coil was used for excitation and signal detection to maximize the uniformity of the images. After localizer scans, a Relaxation Compensated Fat Fraction (RCFF) MRI acquisition and reconstruction process was used to generate quantitative fat fraction maps for each imaging slice [29]. Briefly, three asymmetric echo spin echo MRI acquisitions were acquired (TR/TE = 1500 ms/20 ms, 17–25 coronal slices, resolution = 200 um×200 um×1000 um, 2 averages).…”

Section: Methodsmentioning

confidence: 99%

Caspase-1 as a Central Regulator of High Fat Diet-Induced Non-Alcoholic Steatohepatitis

et al. 2013

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Nonalcoholic steatohepatitis (NASH) is associated with caspase activation. However, a role for pro-inflammatory caspases or inflammasomes has not been explored in diet-induced liver injury. Our aims were to examine the role of caspase-1 in high fat-induced NASH. C57BL/6 wild-type and caspase 1-knockout (Casp1-/-) mice were placed on a 12-week high fat diet. Wild-type mice on the high fat diet increased hepatic expression of pro-caspase-1 and IL-1β. Both wild-type and Casp1-/- mice on the high fat diet gained more weight than mice on a control diet. Hepatic steatosis and TG levels were increased in wild-type mice on high fat diet, but were attenuated in the absence of caspase-1. Plasma cholesterol and free fatty acids were elevated in wild-type, but not Casp1-/- mice, on high fat diet. ALT levels were elevated in both wild-type and Casp1-/- mice on high fat diet compared to control. Hepatic mRNA expression for genes associated with lipogenesis was lower in Casp1-/- mice on high fat diet compared to wild-type mice on high fat diet, while genes associated with fatty acid oxidation were not affected by diet or genotype. Hepatic Tnfα and Mcp-1 mRNA expression was increased in wild-type mice on high fat diet, but not in Casp1-/- mice on high fat diet. αSMA positive cells, Sirius red staining, and Col1α1 mRNA were increased in wild-type mice on high fat diet compared to control. Deficiency of caspase-1 prevented those increases. In summary, the absence of caspase-1 ameliorates the injurious effects of high fat diet-induced obesity on the liver. Specifically, mice deficient in caspase-1 are protected from high fat-induced hepatic steatosis, inflammation and early fibrogenesis. These data point to the inflammasome as an important therapeutic target for NASH.

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“…A similar analysis was performed with a relaxation‐compensated fat fraction (RCFF) , which was calculated as previously described, and as follows:

R C F F = \frac{\frac{true| {normalρ}_{f a t} true|}{true(1 - e^{- T R / T 1_{f a t}} true) e^{- T R / T 2_{f a t}}}}{\frac{true| {normalρ}_{w a t e r} true|}{true(1 - e^{- T R / T 1_{w a t e r}} true) e^{- T R / T 2_{f a t}}} + \frac{true| {normalρ}_{f a t} true|}{true(1 - e^{- T R / T 1_{f a t}} true) e^{- T R / T 2_{f a t}}}}

…”

Section: Methodsmentioning

confidence: 99%

“…The T 1 and T 2 values that were used in the description of RCFF were used here. The nominal TR and TE values, as delineated above, were also used in the calculation.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Hepatic fat during fasting and refeeding by MRI fat quantification

Narayan

Flask

Kalhan

et al. 2014

Magnetic Resonance Imaging

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Purpose To explore the sensitivity of high-field small animal magnetic resonance imaging to dynamic changes in fat content in the liver and to characterize the effect of prandial state on imaging studies of hepatic fat. Materials and Methods A total of 3 time-points were acquired using asymmetric spin-echo acquisitions for 12 mice with 24 hour spacing. After the first scan, half of the cohort was placed on a water-only diet. The second half of the cohort continued to have access to their high-fat chow. The scans were repeated after 24 hours. All animals were then returned to the high-fat diet, and the scans were again repeated after 24 hours. Fat fraction maps were computed using previously described methods. Regions of interests were manually drawn in the livers, and the patterns of the two groups over time were compared. Results Five out of six of the animals in the starved group showed an increase in hepatic fat fraction during the fasting period (average increase 0.54±0.48), which decreased on refeeding. ANOVA analysis indicated that the results significantly depended on both the group and the time-point (p=0.003). Conclusion Fat-water imaging methods are able to measure hepatic fat changes caused by short-term dietary perturbations.

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Body composition analysis of obesity and hepatic steatosis in mice by relaxation compensated fat fraction (RCFF) MRI

Cited by 14 publications

References 25 publications

Obesity‐initiated metabolic syndrome promotes urinary voiding dysfunction in a mouse model

Obesity‐initiated metabolic syndrome promotes urinary voiding dysfunction in a mouse model

Caspase-1 as a Central Regulator of High Fat Diet-Induced Non-Alcoholic Steatohepatitis

Hepatic fat during fasting and refeeding by MRI fat quantification

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