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Reduced white fat mass in adult mice bearing a truncated Patched 1.

Li Z, Zhang H, Denhard LA, Liu LH, Zhou H, Lan ZJ - Int. J. Biol. Sci. (2008)

Bottom Line: Hedgehog (Hh) signaling emerges as a potential pathway contributing to fat formation during postnatal development.Reduced total white fat mass and epididymal adipocyte cell size were observed in naturally occurring spontaneous mesenchymal dysplasia (mes) adult mice (Ptc1(mes/mes)), which carry a deletion of Ptc1 at the carboxyl-terminal cytoplasmic region.Taken together, our results indicate that deletion of carboxyl-terminal tail of Ptc1 can lead to the reduction of white fat mass during postnatal development.

View Article: PubMed Central - PubMed

Affiliation: Birth Defects Center, Department of Molecular, Cellular, Craniofacial Biology, University of Louisville Health Sciences Center, Louisville, KY 40202, USA.

ABSTRACT
Hedgehog (Hh) signaling emerges as a potential pathway contributing to fat formation during postnatal development. In this report, we found that Patched 1 (Ptc1), a negative regulator of Hh signaling, was expressed in the epididymal fat pad of adult mice. Reduced total white fat mass and epididymal adipocyte cell size were observed in naturally occurring spontaneous mesenchymal dysplasia (mes) adult mice (Ptc1(mes/mes)), which carry a deletion of Ptc1 at the carboxyl-terminal cytoplasmic region. Increased expression of truncated Ptc1, Ptc2 and Gli1, the indicators of ectopic activation of Hh signaling, was observed in epididymal fat pads of adult Ptc1(mes/mes) mice. In contrast, expression of peroxisome proliferator-activated receptor gamma, CCAAT/enhancer binding protein alpha, adipocyte P2 and adipsin were reduced in epididymal fat pads of adult Ptc1(mes/mes) mice. Taken together, our results indicate that deletion of carboxyl-terminal tail of Ptc1 can lead to the reduction of white fat mass during postnatal development.

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Reduced total WAT and adipocyte cell sizes in adult male Ptc1mes/mesmice, when compared to control Ptc1+/+ littermates. a-d. Total WAT weights (a), body weights (b), the ratios of total WAT to body weights (c) and major organ weights (d) of Ptc1+/+, Ptc1mes/+ and Ptc1mes/mes male mice during postnatal development. e. Representative photos showing reduced total WAT in Ptc1mes/mesmice. Total WAT of two wild type and their Ptc1mes/mes littermates at the age of 33 weeks are shown. f. Histology of WAT from 33-week-old Ptc1+/+ and Ptc1mes/mes littermates. Note the small adipocyte cell size in WAT of Ptc1mes/mes mice. g. Quantitative analyses showing the reduced cell size of WAT in 33-week-old Ptc1mes/mes mice, when compared to their wild type littermates. In a-d and g, data are presented as mean ± SEM of the indicated numbers of mice in the bar graphs. *P < 0.05, **P < 0.01, when compared to Ptc1+/+ and/or Ptc1mes/+ littermates.
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Figure 2: Reduced total WAT and adipocyte cell sizes in adult male Ptc1mes/mesmice, when compared to control Ptc1+/+ littermates. a-d. Total WAT weights (a), body weights (b), the ratios of total WAT to body weights (c) and major organ weights (d) of Ptc1+/+, Ptc1mes/+ and Ptc1mes/mes male mice during postnatal development. e. Representative photos showing reduced total WAT in Ptc1mes/mesmice. Total WAT of two wild type and their Ptc1mes/mes littermates at the age of 33 weeks are shown. f. Histology of WAT from 33-week-old Ptc1+/+ and Ptc1mes/mes littermates. Note the small adipocyte cell size in WAT of Ptc1mes/mes mice. g. Quantitative analyses showing the reduced cell size of WAT in 33-week-old Ptc1mes/mes mice, when compared to their wild type littermates. In a-d and g, data are presented as mean ± SEM of the indicated numbers of mice in the bar graphs. *P < 0.05, **P < 0.01, when compared to Ptc1+/+ and/or Ptc1mes/+ littermates.

Mentions: To investigate if there is any defect in WAT during postnatal development, total WAT, body and major organ weights of male Ptc1+/+, Ptc1mes/+ and Ptc1mes/mes littermates at various ages were determined (Figure 2). As shown in Figure 2a, total WAT weights were reduced in Ptc1mes/mes male mice during postnatal development with a modest reduction at the age of 19-20 weeks and the remarkable reduction at the age of 33 or 38 weeks, when compared to their wild type and heterozygous littermates (Figure 2a). No significant changes in body weights were observed between male Ptc1mes/mesand control wild type and heterozygous littermates during postnatal development, except that 19-20-week-old Ptc1mes/mesmales were slightly heavier than their controls (Figure 2b). The ratios of total WAT to body weights were also significantly reduced in 19-20-week-old or older Ptc1mes/mes males (Figure 2c). In contrast, there were no significant changes in gross weights of other tested organs including liver, spleen, kidney, lung and heart (Figure 2d). The representative results of reduced total WAT of 33-week-old Ptc1mes/mes male mice were shown in Figure 2e. Histological analyses showed that epididymal fat cells of these Ptc1mes/mes mice were smaller than those of Ptc1+/+ mice (Figure 2f). Quantitative analyses showed that the sizes of epididymal WAT cells in 33-week-old Ptc1mes/mes mice were significantly reduced (P < 0.01), when compared to those of Ptc1+/+littermates (Figure 2g).


Reduced white fat mass in adult mice bearing a truncated Patched 1.

Li Z, Zhang H, Denhard LA, Liu LH, Zhou H, Lan ZJ - Int. J. Biol. Sci. (2008)

Reduced total WAT and adipocyte cell sizes in adult male Ptc1mes/mesmice, when compared to control Ptc1+/+ littermates. a-d. Total WAT weights (a), body weights (b), the ratios of total WAT to body weights (c) and major organ weights (d) of Ptc1+/+, Ptc1mes/+ and Ptc1mes/mes male mice during postnatal development. e. Representative photos showing reduced total WAT in Ptc1mes/mesmice. Total WAT of two wild type and their Ptc1mes/mes littermates at the age of 33 weeks are shown. f. Histology of WAT from 33-week-old Ptc1+/+ and Ptc1mes/mes littermates. Note the small adipocyte cell size in WAT of Ptc1mes/mes mice. g. Quantitative analyses showing the reduced cell size of WAT in 33-week-old Ptc1mes/mes mice, when compared to their wild type littermates. In a-d and g, data are presented as mean ± SEM of the indicated numbers of mice in the bar graphs. *P < 0.05, **P < 0.01, when compared to Ptc1+/+ and/or Ptc1mes/+ littermates.
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Related In: Results  -  Collection

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Figure 2: Reduced total WAT and adipocyte cell sizes in adult male Ptc1mes/mesmice, when compared to control Ptc1+/+ littermates. a-d. Total WAT weights (a), body weights (b), the ratios of total WAT to body weights (c) and major organ weights (d) of Ptc1+/+, Ptc1mes/+ and Ptc1mes/mes male mice during postnatal development. e. Representative photos showing reduced total WAT in Ptc1mes/mesmice. Total WAT of two wild type and their Ptc1mes/mes littermates at the age of 33 weeks are shown. f. Histology of WAT from 33-week-old Ptc1+/+ and Ptc1mes/mes littermates. Note the small adipocyte cell size in WAT of Ptc1mes/mes mice. g. Quantitative analyses showing the reduced cell size of WAT in 33-week-old Ptc1mes/mes mice, when compared to their wild type littermates. In a-d and g, data are presented as mean ± SEM of the indicated numbers of mice in the bar graphs. *P < 0.05, **P < 0.01, when compared to Ptc1+/+ and/or Ptc1mes/+ littermates.
Mentions: To investigate if there is any defect in WAT during postnatal development, total WAT, body and major organ weights of male Ptc1+/+, Ptc1mes/+ and Ptc1mes/mes littermates at various ages were determined (Figure 2). As shown in Figure 2a, total WAT weights were reduced in Ptc1mes/mes male mice during postnatal development with a modest reduction at the age of 19-20 weeks and the remarkable reduction at the age of 33 or 38 weeks, when compared to their wild type and heterozygous littermates (Figure 2a). No significant changes in body weights were observed between male Ptc1mes/mesand control wild type and heterozygous littermates during postnatal development, except that 19-20-week-old Ptc1mes/mesmales were slightly heavier than their controls (Figure 2b). The ratios of total WAT to body weights were also significantly reduced in 19-20-week-old or older Ptc1mes/mes males (Figure 2c). In contrast, there were no significant changes in gross weights of other tested organs including liver, spleen, kidney, lung and heart (Figure 2d). The representative results of reduced total WAT of 33-week-old Ptc1mes/mes male mice were shown in Figure 2e. Histological analyses showed that epididymal fat cells of these Ptc1mes/mes mice were smaller than those of Ptc1+/+ mice (Figure 2f). Quantitative analyses showed that the sizes of epididymal WAT cells in 33-week-old Ptc1mes/mes mice were significantly reduced (P < 0.01), when compared to those of Ptc1+/+littermates (Figure 2g).

Bottom Line: Hedgehog (Hh) signaling emerges as a potential pathway contributing to fat formation during postnatal development.Reduced total white fat mass and epididymal adipocyte cell size were observed in naturally occurring spontaneous mesenchymal dysplasia (mes) adult mice (Ptc1(mes/mes)), which carry a deletion of Ptc1 at the carboxyl-terminal cytoplasmic region.Taken together, our results indicate that deletion of carboxyl-terminal tail of Ptc1 can lead to the reduction of white fat mass during postnatal development.

View Article: PubMed Central - PubMed

Affiliation: Birth Defects Center, Department of Molecular, Cellular, Craniofacial Biology, University of Louisville Health Sciences Center, Louisville, KY 40202, USA.

ABSTRACT
Hedgehog (Hh) signaling emerges as a potential pathway contributing to fat formation during postnatal development. In this report, we found that Patched 1 (Ptc1), a negative regulator of Hh signaling, was expressed in the epididymal fat pad of adult mice. Reduced total white fat mass and epididymal adipocyte cell size were observed in naturally occurring spontaneous mesenchymal dysplasia (mes) adult mice (Ptc1(mes/mes)), which carry a deletion of Ptc1 at the carboxyl-terminal cytoplasmic region. Increased expression of truncated Ptc1, Ptc2 and Gli1, the indicators of ectopic activation of Hh signaling, was observed in epididymal fat pads of adult Ptc1(mes/mes) mice. In contrast, expression of peroxisome proliferator-activated receptor gamma, CCAAT/enhancer binding protein alpha, adipocyte P2 and adipsin were reduced in epididymal fat pads of adult Ptc1(mes/mes) mice. Taken together, our results indicate that deletion of carboxyl-terminal tail of Ptc1 can lead to the reduction of white fat mass during postnatal development.

Show MeSH
Related in: MedlinePlus