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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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Related in: MedlinePlus

No significant change in (a) food intake and (b) glucose tolerance between adult Ptc1mes/mes and their control (Ptc1+/+ or Ptc1mes/+) mice. a. Food consumption by five adult wild type and Ptc1mes/mes mice at the age of 23-27 weeks was recorded weekly for consecutive two weeks. b. Overnight-fasted 24-26-week-old littermates were subjected to glucose tolerance experiments as described in Materials and Methods. Data are presented as mean ± SEM of the indicated numbers of mice in the bar graphs. Student's t-test was performed to determine the significant difference. P value was greater than 0.05 between Ptc1mes/mes and controls (Ptc1+/+ or Ptc1mes/+) at each time point in the figure.
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Figure 4: No significant change in (a) food intake and (b) glucose tolerance between adult Ptc1mes/mes and their control (Ptc1+/+ or Ptc1mes/+) mice. a. Food consumption by five adult wild type and Ptc1mes/mes mice at the age of 23-27 weeks was recorded weekly for consecutive two weeks. b. Overnight-fasted 24-26-week-old littermates were subjected to glucose tolerance experiments as described in Materials and Methods. Data are presented as mean ± SEM of the indicated numbers of mice in the bar graphs. Student's t-test was performed to determine the significant difference. P value was greater than 0.05 between Ptc1mes/mes and controls (Ptc1+/+ or Ptc1mes/+) at each time point in the figure.

Mentions: To determine if there is any difference in food consumption by Ptc1mes/mes and their control Ptc1+/+ mice, we performed food intake experiments. As shown in Figure 4a, there was no statistically significant change in food consumption in either adult Ptc1mes/mes or Ptc1+/+ mice during the consecutive two weeks. The average food intake by adult Ptc1mes/mes mice at each tested week was also not significantly different from Ptc1+/+ control mice (Figure 4a). To test if there is any abnormality in serum glucose concentrations in adult Ptc1mes/mes mice, glucose tolerance experiments were performed. As shown in Figure 4b, no statistical significance of difference in serum glucose concentrations among adult Ptc1+/+, Ptc1mes/+ and Ptc1mes/mes mice at each tested time point after the injections of high doses of glucose.


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)

No significant change in (a) food intake and (b) glucose tolerance between adult Ptc1mes/mes and their control (Ptc1+/+ or Ptc1mes/+) mice. a. Food consumption by five adult wild type and Ptc1mes/mes mice at the age of 23-27 weeks was recorded weekly for consecutive two weeks. b. Overnight-fasted 24-26-week-old littermates were subjected to glucose tolerance experiments as described in Materials and Methods. Data are presented as mean ± SEM of the indicated numbers of mice in the bar graphs. Student's t-test was performed to determine the significant difference. P value was greater than 0.05 between Ptc1mes/mes and controls (Ptc1+/+ or Ptc1mes/+) at each time point in the figure.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2238183&req=5

Figure 4: No significant change in (a) food intake and (b) glucose tolerance between adult Ptc1mes/mes and their control (Ptc1+/+ or Ptc1mes/+) mice. a. Food consumption by five adult wild type and Ptc1mes/mes mice at the age of 23-27 weeks was recorded weekly for consecutive two weeks. b. Overnight-fasted 24-26-week-old littermates were subjected to glucose tolerance experiments as described in Materials and Methods. Data are presented as mean ± SEM of the indicated numbers of mice in the bar graphs. Student's t-test was performed to determine the significant difference. P value was greater than 0.05 between Ptc1mes/mes and controls (Ptc1+/+ or Ptc1mes/+) at each time point in the figure.
Mentions: To determine if there is any difference in food consumption by Ptc1mes/mes and their control Ptc1+/+ mice, we performed food intake experiments. As shown in Figure 4a, there was no statistically significant change in food consumption in either adult Ptc1mes/mes or Ptc1+/+ mice during the consecutive two weeks. The average food intake by adult Ptc1mes/mes mice at each tested week was also not significantly different from Ptc1+/+ control mice (Figure 4a). To test if there is any abnormality in serum glucose concentrations in adult Ptc1mes/mes mice, glucose tolerance experiments were performed. As shown in Figure 4b, no statistical significance of difference in serum glucose concentrations among adult Ptc1+/+, Ptc1mes/+ and Ptc1mes/mes mice at each tested time point after the injections of high doses of glucose.

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