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High-fat diet-induced adiposity, adipose inflammation, hepatic steatosis and hyperinsulinemia in outbred CD-1 mice.

Gao M, Ma Y, Liu D - PLoS ONE (2015)

Bottom Line: Increased fat accumulation in white adipose tissue subsequently led to ectopic fat deposition in brown adipose tissue, giving rise to whitening of brown adipose tissue without altering plasma level of triglyceride.Ectopic fat deposition was also observed in the liver, which was associated with elevated expression of key genes involved in hepatic lipid sequestration, including Ppar-γ2, Cd36 and Mgat1.Notably, adipose chronic inflammation and ectopic lipid deposition in the liver and brown fat were accompanied by glucose intolerance and insulin resistance, which was correlated with hyperinsulinemia and pancreatic islet hypertrophy.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, Georgia, United States of America.

ABSTRACT
High-fat diet (HFD) has been applied to a variety of inbred mouse strains to induce obesity and obesity related metabolic complications. In this study, we determined HFD induced development of metabolic disorders on outbred female CD-1 mice in a time dependent manner. Compared to mice on regular chow, HFD-fed CD-1 mice gradually gained more fat mass and consequently exhibited accelerated body weight gain, which was associated with adipocyte hypertrophy and up-regulated expression of adipose inflammatory chemokines and cytokines such as Mcp-1 and Tnf-α. Increased fat accumulation in white adipose tissue subsequently led to ectopic fat deposition in brown adipose tissue, giving rise to whitening of brown adipose tissue without altering plasma level of triglyceride. Ectopic fat deposition was also observed in the liver, which was associated with elevated expression of key genes involved in hepatic lipid sequestration, including Ppar-γ2, Cd36 and Mgat1. Notably, adipose chronic inflammation and ectopic lipid deposition in the liver and brown fat were accompanied by glucose intolerance and insulin resistance, which was correlated with hyperinsulinemia and pancreatic islet hypertrophy. Collectively, these results demonstrate sequentially the events that HFD induces physiological changes leading to metabolic disorders in an outbred mouse model more closely resembling heterogeneity of the human population.

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HFD increased body weight gain in female CD-1 mice.(A) Growth curve of mice on HFD or chow. (B) Representative images of mice (bar length = 1 cm). (C) Energy intake. Values in (A) and (C) represent average ± SD (n = 10). * P < 0.05 compared with mice on chow, ** P < 0.01 compared with mice on chow.
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pone.0119784.g001: HFD increased body weight gain in female CD-1 mice.(A) Growth curve of mice on HFD or chow. (B) Representative images of mice (bar length = 1 cm). (C) Energy intake. Values in (A) and (C) represent average ± SD (n = 10). * P < 0.05 compared with mice on chow, ** P < 0.01 compared with mice on chow.

Mentions: To investigate whether HFD accelerated body weight gain in female CD-1 mice, we compared 2 groups (n = 10 per group) of animals fed either an HFD or regular chow for 12 weeks. Fig. 1A shows that compared to regular chow, the HFD greatly accelerated body weight gain in these mice. The average growth rate for mice on the HFD is ∼1.4 g/week while that on a regular chow is merely ∼0.4 g/week. At the end of the experiment, the difference in body weight gain between the 2 groups reached ∼11.8 g (Fig. 1A). The difference became significant on week 4 and can be easily recognized visually starting on week 8 (Fig. 1A-B). The average energy intake was ∼14.3 and ∼14.9 kcal/mouse/day for mice on chow or HFD, respectively (Fig. 1C). This set of data demonstrates that HFD accelerates body weight gain in female CD-1 mice.


High-fat diet-induced adiposity, adipose inflammation, hepatic steatosis and hyperinsulinemia in outbred CD-1 mice.

Gao M, Ma Y, Liu D - PLoS ONE (2015)

HFD increased body weight gain in female CD-1 mice.(A) Growth curve of mice on HFD or chow. (B) Representative images of mice (bar length = 1 cm). (C) Energy intake. Values in (A) and (C) represent average ± SD (n = 10). * P < 0.05 compared with mice on chow, ** P < 0.01 compared with mice on chow.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4358885&req=5

pone.0119784.g001: HFD increased body weight gain in female CD-1 mice.(A) Growth curve of mice on HFD or chow. (B) Representative images of mice (bar length = 1 cm). (C) Energy intake. Values in (A) and (C) represent average ± SD (n = 10). * P < 0.05 compared with mice on chow, ** P < 0.01 compared with mice on chow.
Mentions: To investigate whether HFD accelerated body weight gain in female CD-1 mice, we compared 2 groups (n = 10 per group) of animals fed either an HFD or regular chow for 12 weeks. Fig. 1A shows that compared to regular chow, the HFD greatly accelerated body weight gain in these mice. The average growth rate for mice on the HFD is ∼1.4 g/week while that on a regular chow is merely ∼0.4 g/week. At the end of the experiment, the difference in body weight gain between the 2 groups reached ∼11.8 g (Fig. 1A). The difference became significant on week 4 and can be easily recognized visually starting on week 8 (Fig. 1A-B). The average energy intake was ∼14.3 and ∼14.9 kcal/mouse/day for mice on chow or HFD, respectively (Fig. 1C). This set of data demonstrates that HFD accelerates body weight gain in female CD-1 mice.

Bottom Line: Increased fat accumulation in white adipose tissue subsequently led to ectopic fat deposition in brown adipose tissue, giving rise to whitening of brown adipose tissue without altering plasma level of triglyceride.Ectopic fat deposition was also observed in the liver, which was associated with elevated expression of key genes involved in hepatic lipid sequestration, including Ppar-γ2, Cd36 and Mgat1.Notably, adipose chronic inflammation and ectopic lipid deposition in the liver and brown fat were accompanied by glucose intolerance and insulin resistance, which was correlated with hyperinsulinemia and pancreatic islet hypertrophy.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, University of Georgia, Athens, Georgia, United States of America.

ABSTRACT
High-fat diet (HFD) has been applied to a variety of inbred mouse strains to induce obesity and obesity related metabolic complications. In this study, we determined HFD induced development of metabolic disorders on outbred female CD-1 mice in a time dependent manner. Compared to mice on regular chow, HFD-fed CD-1 mice gradually gained more fat mass and consequently exhibited accelerated body weight gain, which was associated with adipocyte hypertrophy and up-regulated expression of adipose inflammatory chemokines and cytokines such as Mcp-1 and Tnf-α. Increased fat accumulation in white adipose tissue subsequently led to ectopic fat deposition in brown adipose tissue, giving rise to whitening of brown adipose tissue without altering plasma level of triglyceride. Ectopic fat deposition was also observed in the liver, which was associated with elevated expression of key genes involved in hepatic lipid sequestration, including Ppar-γ2, Cd36 and Mgat1. Notably, adipose chronic inflammation and ectopic lipid deposition in the liver and brown fat were accompanied by glucose intolerance and insulin resistance, which was correlated with hyperinsulinemia and pancreatic islet hypertrophy. Collectively, these results demonstrate sequentially the events that HFD induces physiological changes leading to metabolic disorders in an outbred mouse model more closely resembling heterogeneity of the human population.

Show MeSH
Related in: MedlinePlus