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Tracing the movement of adiponectin in a parabiosis model of wild-type and adiponectin-knockout mice.

Nakatsuji H, Kishida K, Sekimoto R, Funahashi T, Shimomura I - FEBS Open Bio (2014)

Bottom Line: Hypoadiponectinemia is associated in obese individuals with insulin resistance and atherosclerosis.In the WT-KO parabiosis model, circulating adiponectin levels of the WT partners decreased rapidly, on the other hand, those of KO partners increased, and then these reached comparable levels each other at day 7.In the diet-induced obesity model, high adiponectin protein levels were detected in adipose stromal vascular fraction of diet-induced obese KO partner, without changes in its binding proteins.

View Article: PubMed Central - PubMed

Affiliation: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.

ABSTRACT
Adiponectin is exclusively synthesized by adipocytes and exhibits anti-diabetic, anti-atherosclerotic and anti-inflammatory properties. Hypoadiponectinemia is associated in obese individuals with insulin resistance and atherosclerosis. However, the mechanisms responsible for hypoadiponectinemia remain unclear. Here, we investigated adiponectin movement using hetero parabiosis model of wild type (WT) and adiponectin-deficient (KO) mice. WT mice were parabiosed with WT mice (WT-WT) or KO mice (WT-KO) and adiponectin levels were measured serially up to 63 days after surgery. In the WT-KO parabiosis model, circulating adiponectin levels of the WT partners decreased rapidly, on the other hand, those of KO partners increased, and then these reached comparable levels each other at day 7. Circulating adiponectin levels decreased further to the detection limit of assay, and remained low up to day 63. However, adiponectin protein was detected in the adipose tissues of not only the WT partner but also WT-KO mice. In the diet-induced obesity model, high adiponectin protein levels were detected in adipose stromal vascular fraction of diet-induced obese KO partner, without changes in its binding proteins. The use of parabiosis experiments shed light on movement of native adiponectin among different tissues such as the state of hypoadiponectinemia in obesity.

No MeSH data available.


Related in: MedlinePlus

Diet-induced obese parabiotic mice. (A) Experimental protocol. WT mice were parabiosed with KO mice (WT–KO). Starting day 8, mice were fed either normal chow (NC, n = 8) or high fat/high sucrose diet (HF/HS, n = 16) for 8 weeks. At 63 days, the mice were sacrificed and their tissues analyzed. (B) Body weight of a pair of parabiosed mice. Plasma adiponectin levels were measured by ELISA in partners of parabiosed mice (bottom). (C) Effect of obesity on blood glucose, insulin and serum adiponectin. Data are mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001; NC- vs. HF/HS-fed WT (WT–KO) mice (C), #p < 0.05, ##p < 0.01, NC vs. HF/HS fed KO (WT–KO) mice (C). Each experiment was repeated at least three times.
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f0015: Diet-induced obese parabiotic mice. (A) Experimental protocol. WT mice were parabiosed with KO mice (WT–KO). Starting day 8, mice were fed either normal chow (NC, n = 8) or high fat/high sucrose diet (HF/HS, n = 16) for 8 weeks. At 63 days, the mice were sacrificed and their tissues analyzed. (B) Body weight of a pair of parabiosed mice. Plasma adiponectin levels were measured by ELISA in partners of parabiosed mice (bottom). (C) Effect of obesity on blood glucose, insulin and serum adiponectin. Data are mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001; NC- vs. HF/HS-fed WT (WT–KO) mice (C), #p < 0.05, ##p < 0.01, NC vs. HF/HS fed KO (WT–KO) mice (C). Each experiment was repeated at least three times.

Mentions: Does adiponectin protein accumulate in WAT of obese mice more than that of lean mice after long-term adiponectin recruitment? To answer this question, we compared high fat/high sucrose (HF/HS) diet-induced obese parabiosis WT and APN-KO mice and parabiosis mice fed NC diet (Fig. 3A, B). HF/HS diet load was provided at day 8 after operation, based on the finding of comparable levels of plasma adiponectin levels at day 7 (Fig. 3C bottom). The body weight of parabiotic partners slightly, but significantly, increased during the 8-week period of HF/HS feeding (Fig. 3B). Plasma glucose levels were significantly higher in WT (WT–KO) fed HF/HS than WT (WT–KO) fed NC at days 14 and 21 (p = 0.0006, p < 0.0001 each), however, no such difference was observed at day 63. Plasma insulin levels were significantly higher in HF/HS-fed mice than in NC-fed mice [WT (WT–KO) fed NC vs. WT (WT–KO) fed HF/HS; p = 0.0094 at day 14, p = 0.0222 at day 21, p = 0.0256 at day 63, KO (WT–KO) fed NC vs. KO (WT–KO) fed HF/HS; p = 0.0070 at day 14, p = 0.0079 at day 21, p = 0.0120 at day 63]. In the HF/HS fed mice, plasma insulin levels were higher in WT (WT-KO) than in KO (WT-KO). These data suggest that adiponectin derived from WT (WT-KO) seems to improve insulin resistance in KO (WT-KO), which lack native adiponectin.


Tracing the movement of adiponectin in a parabiosis model of wild-type and adiponectin-knockout mice.

Nakatsuji H, Kishida K, Sekimoto R, Funahashi T, Shimomura I - FEBS Open Bio (2014)

Diet-induced obese parabiotic mice. (A) Experimental protocol. WT mice were parabiosed with KO mice (WT–KO). Starting day 8, mice were fed either normal chow (NC, n = 8) or high fat/high sucrose diet (HF/HS, n = 16) for 8 weeks. At 63 days, the mice were sacrificed and their tissues analyzed. (B) Body weight of a pair of parabiosed mice. Plasma adiponectin levels were measured by ELISA in partners of parabiosed mice (bottom). (C) Effect of obesity on blood glucose, insulin and serum adiponectin. Data are mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001; NC- vs. HF/HS-fed WT (WT–KO) mice (C), #p < 0.05, ##p < 0.01, NC vs. HF/HS fed KO (WT–KO) mice (C). Each experiment was repeated at least three times.
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Related In: Results  -  Collection

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f0015: Diet-induced obese parabiotic mice. (A) Experimental protocol. WT mice were parabiosed with KO mice (WT–KO). Starting day 8, mice were fed either normal chow (NC, n = 8) or high fat/high sucrose diet (HF/HS, n = 16) for 8 weeks. At 63 days, the mice were sacrificed and their tissues analyzed. (B) Body weight of a pair of parabiosed mice. Plasma adiponectin levels were measured by ELISA in partners of parabiosed mice (bottom). (C) Effect of obesity on blood glucose, insulin and serum adiponectin. Data are mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001; NC- vs. HF/HS-fed WT (WT–KO) mice (C), #p < 0.05, ##p < 0.01, NC vs. HF/HS fed KO (WT–KO) mice (C). Each experiment was repeated at least three times.
Mentions: Does adiponectin protein accumulate in WAT of obese mice more than that of lean mice after long-term adiponectin recruitment? To answer this question, we compared high fat/high sucrose (HF/HS) diet-induced obese parabiosis WT and APN-KO mice and parabiosis mice fed NC diet (Fig. 3A, B). HF/HS diet load was provided at day 8 after operation, based on the finding of comparable levels of plasma adiponectin levels at day 7 (Fig. 3C bottom). The body weight of parabiotic partners slightly, but significantly, increased during the 8-week period of HF/HS feeding (Fig. 3B). Plasma glucose levels were significantly higher in WT (WT–KO) fed HF/HS than WT (WT–KO) fed NC at days 14 and 21 (p = 0.0006, p < 0.0001 each), however, no such difference was observed at day 63. Plasma insulin levels were significantly higher in HF/HS-fed mice than in NC-fed mice [WT (WT–KO) fed NC vs. WT (WT–KO) fed HF/HS; p = 0.0094 at day 14, p = 0.0222 at day 21, p = 0.0256 at day 63, KO (WT–KO) fed NC vs. KO (WT–KO) fed HF/HS; p = 0.0070 at day 14, p = 0.0079 at day 21, p = 0.0120 at day 63]. In the HF/HS fed mice, plasma insulin levels were higher in WT (WT-KO) than in KO (WT-KO). These data suggest that adiponectin derived from WT (WT-KO) seems to improve insulin resistance in KO (WT-KO), which lack native adiponectin.

Bottom Line: Hypoadiponectinemia is associated in obese individuals with insulin resistance and atherosclerosis.In the WT-KO parabiosis model, circulating adiponectin levels of the WT partners decreased rapidly, on the other hand, those of KO partners increased, and then these reached comparable levels each other at day 7.In the diet-induced obesity model, high adiponectin protein levels were detected in adipose stromal vascular fraction of diet-induced obese KO partner, without changes in its binding proteins.

View Article: PubMed Central - PubMed

Affiliation: Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.

ABSTRACT
Adiponectin is exclusively synthesized by adipocytes and exhibits anti-diabetic, anti-atherosclerotic and anti-inflammatory properties. Hypoadiponectinemia is associated in obese individuals with insulin resistance and atherosclerosis. However, the mechanisms responsible for hypoadiponectinemia remain unclear. Here, we investigated adiponectin movement using hetero parabiosis model of wild type (WT) and adiponectin-deficient (KO) mice. WT mice were parabiosed with WT mice (WT-WT) or KO mice (WT-KO) and adiponectin levels were measured serially up to 63 days after surgery. In the WT-KO parabiosis model, circulating adiponectin levels of the WT partners decreased rapidly, on the other hand, those of KO partners increased, and then these reached comparable levels each other at day 7. Circulating adiponectin levels decreased further to the detection limit of assay, and remained low up to day 63. However, adiponectin protein was detected in the adipose tissues of not only the WT partner but also WT-KO mice. In the diet-induced obesity model, high adiponectin protein levels were detected in adipose stromal vascular fraction of diet-induced obese KO partner, without changes in its binding proteins. The use of parabiosis experiments shed light on movement of native adiponectin among different tissues such as the state of hypoadiponectinemia in obesity.

No MeSH data available.


Related in: MedlinePlus