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Targeting TRPV1 for Body Weight Control using TRPV1(-/-) Mice and Electroacupuncture.

Choowanthanapakorn M, Lu KW, Yang J, Hsieh CL, Lin YW - Sci Rep (2015)

Bottom Line: The results demonstrated that body weight increased with time in the control group (108.19 ± 1.31%, n = 7).EA did not decrease the gain of body weight in TRPV1 knock mice (107.94 ± 0.41% and 107.79 ± 1.04% for TRPV1(-/-) and TRPV1(-/-) with EA, respectively, p > 0.05).The visceral white adipose tissue (WAT) weight was lower in the EA group at 4 weeks after manipulation.

View Article: PubMed Central - PubMed

Affiliation: College of Chinese Medicine, Graduate Institute of Acupuncture Science and International Master Program, China Medical University, Taichung 40402, Taiwan.

ABSTRACT
Obesity is a global social medical problem resulting in morbidity as high as 20-30%. Here we investigated whether the manipulation of TRPV1 can control mice body weight through electroacupuncture (EA). The results demonstrated that body weight increased with time in the control group (108.19 ± 1.31%, n = 7). The increase of mice body weight was significantly less in the EA group (104.41 ± 0.76%, p < 0.05, compared with the control group, n = 7) but not in the sham EA group (109.1 ± 0.63%, p < 0.05, compared with EA group, n = 7). EA did not decrease the gain of body weight in TRPV1 knock mice (107.94 ± 0.41% and 107.79 ± 1.04% for TRPV1(-/-) and TRPV1(-/-) with EA, respectively, p > 0.05). The visceral white adipose tissue (WAT) weight was lower in the EA group at 4 weeks after manipulation. Moreover, the protein levels of TRPV1, pPKA, pPKC, and pERK were increased in the dorsal root ganglion (DRG) and spinal cord (SC) after EA treatment but not in the sham EA and TRPV1(-/-) mice. This study suggests that targeting TRPV1 is beneficial in controlling body weight and TRPV1-associated mechanisms in mice.

No MeSH data available.


Related in: MedlinePlus

Upregulation of TRPV1 and related signal mechanisms in DRG neurons from EA but not sham mice.(A) Western blot staining showed TRPV1-positive band; (B) pPKA-positive band; (C) pPKC-positive band; (D) pERK-positive band; (E) pp38-positive band; (F) pJNK-positive band in Con, EA, sham groups. Con = control; EA = electroacupuncture; sham = sham-EA group.
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f3: Upregulation of TRPV1 and related signal mechanisms in DRG neurons from EA but not sham mice.(A) Western blot staining showed TRPV1-positive band; (B) pPKA-positive band; (C) pPKC-positive band; (D) pERK-positive band; (E) pp38-positive band; (F) pJNK-positive band in Con, EA, sham groups. Con = control; EA = electroacupuncture; sham = sham-EA group.

Mentions: We tested the effects of EA at ST36 acupoint on the expression of TRPV1 in DRG through western blotting. The expression level of TRPV1 was normal in the control mice (Fig. 3, 100%, n = 7). The results showed that the protein level of TRPV1 was significantly increased after EA treatment at week 4 (Fig. 3, 128.47 ± 5.19%, p < 0.05, compared with the control group, n = 7). The phenomenon was not observed in sham-EA mice (Fig. 3, 100.1 ± 3.21%, p < 0.05, compared with the EA group, n = 7). Because TRPV1 is a Ca2+ permeable ion channel, which can trigger second messenger molecules, we further examined if EA can activate TRPV1 and the related mechanisms. It was observed that the protein level of pPKA was increased in the EA-treated mice (Fig. 3, 116.1 ± 2.44%, p < 0.05, compared to the control group, n = 7) but not in the sham-EA group (Fig. 3, 107.47 ± 9.68%, p < 0.05, compared to the control group, n = 7). Similar results were also obtained in the pPKC protein level suggesting its role in EA-mediated mechanisms (Fig. 3, 180.35 ± 26.48% and 100.95 ± 3.66% for EA and sham EA, respectively, p < 0.05, n = 7). We further assessed if pPKA and pPKC could trigger MAPK family. The results revealed that the protein level of pERK was significantly increased after EA treatment (Fig. 3, 175.91 ± 30.59%, p < 0.05, compared to the control group, n = 7) but not in the sham control mice (Fig. 3, 98.98 ± 7.03%, p < 0.05, compared to the EA group, n = 7). These results were not observed in other members of the MAPK family such as pp38 (Fig. 3, 97.73 ± 5.95% and 97.73 ± 6.77% for EA and sham-EA group, respectively, p < 0.05, n = 7) and pJNK, indicating that pERK is a key element in EA manipulation (Fig. 3, 100.29 ± 2.06% and 101.88 ± 4.71% for EA and sham-EA group, respectively, p < 0.05, n = 7).


Targeting TRPV1 for Body Weight Control using TRPV1(-/-) Mice and Electroacupuncture.

Choowanthanapakorn M, Lu KW, Yang J, Hsieh CL, Lin YW - Sci Rep (2015)

Upregulation of TRPV1 and related signal mechanisms in DRG neurons from EA but not sham mice.(A) Western blot staining showed TRPV1-positive band; (B) pPKA-positive band; (C) pPKC-positive band; (D) pERK-positive band; (E) pp38-positive band; (F) pJNK-positive band in Con, EA, sham groups. Con = control; EA = electroacupuncture; sham = sham-EA group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4664894&req=5

f3: Upregulation of TRPV1 and related signal mechanisms in DRG neurons from EA but not sham mice.(A) Western blot staining showed TRPV1-positive band; (B) pPKA-positive band; (C) pPKC-positive band; (D) pERK-positive band; (E) pp38-positive band; (F) pJNK-positive band in Con, EA, sham groups. Con = control; EA = electroacupuncture; sham = sham-EA group.
Mentions: We tested the effects of EA at ST36 acupoint on the expression of TRPV1 in DRG through western blotting. The expression level of TRPV1 was normal in the control mice (Fig. 3, 100%, n = 7). The results showed that the protein level of TRPV1 was significantly increased after EA treatment at week 4 (Fig. 3, 128.47 ± 5.19%, p < 0.05, compared with the control group, n = 7). The phenomenon was not observed in sham-EA mice (Fig. 3, 100.1 ± 3.21%, p < 0.05, compared with the EA group, n = 7). Because TRPV1 is a Ca2+ permeable ion channel, which can trigger second messenger molecules, we further examined if EA can activate TRPV1 and the related mechanisms. It was observed that the protein level of pPKA was increased in the EA-treated mice (Fig. 3, 116.1 ± 2.44%, p < 0.05, compared to the control group, n = 7) but not in the sham-EA group (Fig. 3, 107.47 ± 9.68%, p < 0.05, compared to the control group, n = 7). Similar results were also obtained in the pPKC protein level suggesting its role in EA-mediated mechanisms (Fig. 3, 180.35 ± 26.48% and 100.95 ± 3.66% for EA and sham EA, respectively, p < 0.05, n = 7). We further assessed if pPKA and pPKC could trigger MAPK family. The results revealed that the protein level of pERK was significantly increased after EA treatment (Fig. 3, 175.91 ± 30.59%, p < 0.05, compared to the control group, n = 7) but not in the sham control mice (Fig. 3, 98.98 ± 7.03%, p < 0.05, compared to the EA group, n = 7). These results were not observed in other members of the MAPK family such as pp38 (Fig. 3, 97.73 ± 5.95% and 97.73 ± 6.77% for EA and sham-EA group, respectively, p < 0.05, n = 7) and pJNK, indicating that pERK is a key element in EA manipulation (Fig. 3, 100.29 ± 2.06% and 101.88 ± 4.71% for EA and sham-EA group, respectively, p < 0.05, n = 7).

Bottom Line: The results demonstrated that body weight increased with time in the control group (108.19 ± 1.31%, n = 7).EA did not decrease the gain of body weight in TRPV1 knock mice (107.94 ± 0.41% and 107.79 ± 1.04% for TRPV1(-/-) and TRPV1(-/-) with EA, respectively, p > 0.05).The visceral white adipose tissue (WAT) weight was lower in the EA group at 4 weeks after manipulation.

View Article: PubMed Central - PubMed

Affiliation: College of Chinese Medicine, Graduate Institute of Acupuncture Science and International Master Program, China Medical University, Taichung 40402, Taiwan.

ABSTRACT
Obesity is a global social medical problem resulting in morbidity as high as 20-30%. Here we investigated whether the manipulation of TRPV1 can control mice body weight through electroacupuncture (EA). The results demonstrated that body weight increased with time in the control group (108.19 ± 1.31%, n = 7). The increase of mice body weight was significantly less in the EA group (104.41 ± 0.76%, p < 0.05, compared with the control group, n = 7) but not in the sham EA group (109.1 ± 0.63%, p < 0.05, compared with EA group, n = 7). EA did not decrease the gain of body weight in TRPV1 knock mice (107.94 ± 0.41% and 107.79 ± 1.04% for TRPV1(-/-) and TRPV1(-/-) with EA, respectively, p > 0.05). The visceral white adipose tissue (WAT) weight was lower in the EA group at 4 weeks after manipulation. Moreover, the protein levels of TRPV1, pPKA, pPKC, and pERK were increased in the dorsal root ganglion (DRG) and spinal cord (SC) after EA treatment but not in the sham EA and TRPV1(-/-) mice. This study suggests that targeting TRPV1 is beneficial in controlling body weight and TRPV1-associated mechanisms in mice.

No MeSH data available.


Related in: MedlinePlus