A Mouse Model of Diet-Induced Obesity and Insulin Resistance

Wang, Chao-Yung; Liao, James K.

doi:10.1007/978-1-61779-430-8_27

Cited by 406 publications

(329 citation statements)

References 19 publications

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“…The particular HFD we selected has been well established to induce hepatic steatosis in a number of mouse strains (61,62). As expected, at the end of the 8-wk feeding period, the HFD mice showed significant increases in body weight (ca.…”

Section: Ccl-1 Reveals Copper Deficiency With Alterations In Copper Tsupporting

confidence: 54%

“…document significant glucose intolerance and metabolic changes in similar diet-dependent mouse models at this time point (61,62). As an additional control, because of differences in copper in normal diet and HFD, parallel experiments were performed in L-Luc mice fed low-fat diets (LFDs) with equivalent copper levels to the HFD.…”

Section: Ccl-1 Reveals Copper Deficiency With Alterations In Copper Tmentioning

confidence: 99%

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In vivo bioluminescence imaging reveals copper deficiency in a murine model of nonalcoholic fatty liver disease

Heffern

Park

Au‐Yeung

et al. 2016

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

149

150

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Copper is a required metal nutrient for life, but global or local alterations in its homeostasis are linked to diseases spanning genetic and metabolic disorders to cancer and neurodegeneration. Technologies that enable longitudinal in vivo monitoring of dynamic copper pools can help meet the need to study the complex interplay between copper status, health, and disease in the same living organism over time. Here, we present the synthesis, characterization, and in vivo imaging applications of Copper-Caged Luciferin-1 (CCL-1), a bioluminescent reporter for tissue-specific copper visualization in living animals. CCL-1 uses a selective copper(I)-dependent oxidative cleavage reaction to release d-luciferin for subsequent bioluminescent reaction with firefly luciferase. The probe can detect physiological changes in labile Cu+ levels in live cells and mice under situations of copper deficiency or overload. Application of CCL-1 to mice with liver-specific luciferase expression in a diet-induced model of nonalcoholic fatty liver disease reveals onset of hepatic copper deficiency and altered expression levels of central copper trafficking proteins that accompany symptoms of glucose intolerance and weight gain. The data connect copper dysregulation to metabolic liver disease and provide a starting point for expanding the toolbox of reactivity-based chemical reporters for cell- and tissue-specific in vivo imaging.

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Section: Ccl-1 Reveals Copper Deficiency With Alterations In Copper Tsupporting

confidence: 54%

Section: Ccl-1 Reveals Copper Deficiency With Alterations In Copper Tmentioning

confidence: 99%

In vivo bioluminescence imaging reveals copper deficiency in a murine model of nonalcoholic fatty liver disease

Heffern

Park

Au‐Yeung

et al. 2016

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

149

150

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“…The observed change in total body mass in the mixed diet group (HF þ SK) was consistently greater than in the 60% fat only group and was also consistent with the profile that has been reported with cafeteria diets. [3][4][5]8,9,16 Interestingly, our mixed diet enhanced the increase in fat mass despite a similar caloric intake between groups. Like the cafeteria diet, our mixed approach may have enhanced weight gain by providing variety.…”

mentioning

confidence: 77%

Considerations to maximize fat mass gain in a mouse model of diet-induced weight gain

2013

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Mouse experimental models of diet-induced weight gain are commonly used as analogs to human obesity; however, a wide variety of feeding methods have been used and the most effective way to maximize weight gain is not known. Maximizing weight gain may allow for a reduction in the number of animals required for a given experiment. The purpose of this study was how to cause the greatest amount of weight gain in CD-1 mice by modifying the composition and source of their diet. To accomplish this goal, we completed two experiments: (1) Effect of dietary macronutrient fat intake (60% (HF60), 45% (HF45), 30% (HF30), or 13.5% (CON) fat diet for 18 weeks); and (2) Effect of 1:1 mixed HF60 and CON diets. Outcome measures included food intake, body mass, and body composition, which were measured bi-weekly and statistically analyzed using a repeated measures analysis of variance (RM-ANOVA). In Experiment 1, the greatest increase in body and fat mass was observed in HF60 (36%) and HF45 (29%) compared with HF30 and CON (P < 0.05). In Experiment 2, HF þ stock diet (SK) gained 25% more body mass and 70% more fat mass than HF (P < 0.05). Collectively, these findings suggest that using a high-fat based diet (>45% calories from fat), mixed with a stock diet, results in substantially more weight gain over a similar period, of time, which would allow an investigator to use $40% fewer animals in their experimental model. Keywords mouse diet-induced weight gain, dietary fat, obesity, disease, mixed dietsIn the past decade, the prevalence of overweight/obesity has reached epidemic levels in many parts of the world, resulting in a rise in morbidity and premature mortality.1,2 Studying the longitudinal effects of dietinduced weight gain in humans is problematic due to ethical considerations. Thus, rodent weight gain models are an attractive analog for human obesity. One limitation of the current studies is that a wide variety of weight gain methodology has been used and it is not clear which method most effectively maximizes weight gain. [3][4][5][6][7][8][9] Through a series of investigations, our laboratory has sought to address this limitation in the current literature. We have previously demonstrated that mice that are group-housed (groups of five) and restricted from structured physical activity have greater weight gain than normal growth rates.10,11 Consistent with reports from other laboratories, we have also demonstrated that extremely high-fat diets (60% of calories from fat) result in excessive weight gain above normal growth.10 Neither our laboratory nor others have specifically compartmentalized weight gain into lean and

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“…Diet modification play important role in the incidence of obesity and its related disorders [19,20]. However, the major contributing factor for obesity is excessive caloric intake, availability of energy-dense meals, urbanization and sedentary life style [21].…”

Section: Discussionmentioning

confidence: 99%

Effect of antioxidant rich nutraceuticals on histological changes due to high fat diet induced obesity in rats

Isa¹,

Abubakar²,

Abubakar³

et al. 2017

Am J Res Med Sci

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Objective: Obesity is an important, multifaceted chronic disorder which has become one of the leading health problems globally as a result of its morbidity and mortality. The aim of this research was to induce obesity using high fat diet feeding and to assess the effect of treatment with antioxidant rich nutraceuticals in the pathology of the liver, kidney and heart. Methods: Nutraceuticals were formulated using locally available foodstuffs (onions, garlic, tomatoes, lemon, palm oil and crayfish in the ratio of 5:5:2:4:2:2) based on recommended daily allowances (RDA). Obesity was induced using high fat diet feeding for ten weeks. Albino rats of both sexes weighing 150-220 g were used for the study. The animals were grouped into 4 group of 8 rats each: group I: normal, control; group II: high fat diet, untreated; group III: high fat diet treated with 250 mg of nutraceutical daily; group IV: high fat diet treated with 500 mg of nutraceutical daily for ten weeks. Sections of liver, kidney and heart were taken for histopathological study. Results:The data obtained showed that high fat diet feeding significantly increased body mass and body mass index and was associated with an abnormal lipid distribution. Histopathological examination showed that high fat diet feeding was associated with hepatic, myocardial and renal necrosis, degeneration and congestion of associated blood vessels. However, treatment with antioxidant rich nutraceutical reverses the damage to near normal. Conclusion: High fat diet induced obesity is associated with pathological changes in the heart, kidney and liver. Antioxidant rich nutraceuticals could provide a protective effect against pathological changes in obesity. ARTICLE HISTORY

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A Mouse Model of Diet-Induced Obesity and Insulin Resistance

Cited by 406 publications

References 19 publications

In vivo bioluminescence imaging reveals copper deficiency in a murine model of nonalcoholic fatty liver disease

In vivo bioluminescence imaging reveals copper deficiency in a murine model of nonalcoholic fatty liver disease

Considerations to maximize fat mass gain in a mouse model of diet-induced weight gain

Effect of antioxidant rich nutraceuticals on histological changes due to high fat diet induced obesity in rats

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