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. 2016 Aug 16:60:31690.
doi: 10.3402/fnr.v60.31690. eCollection 2016.

Effects of cereal fiber on leptin resistance and sensitivity in C57BL/6J mice fed a high-fat/cholesterol diet

Affiliations

Effects of cereal fiber on leptin resistance and sensitivity in C57BL/6J mice fed a high-fat/cholesterol diet

Ru Zhang et al. Food Nutr Res. .

Abstract

Background: Cereal fiber is reported to be associated with obesity and metabolic diseases. However, whether cereal fiber improves leptin resistance and sensitivity remains unclear.

Design: For 24 weeks, 48 male C57BL/6J mice were randomly given a normal chow diet (Chow), high-fat/cholesterol diet (HFD), HFD with 0.8% oat fiber (H-oat) or HFD with 0.8% wheat bran fiber (H-wheat). At the end of feeding period, both the serum insulin and leptin levels were determined by ELISA kits. Western blotting was used to assess the protein expressions of the leptin receptor (LepR) and the leptin-signaling pathway in the adipose tissues.

Results: Our results suggested that mice fed oat or wheat bran fiber exhibited lower body weight, serum lipids, as well as insulin and leptin levels. The two cereal fibers potently increased the protein expressions of LepR in the adipose tissue. In addition, protein expressions of Janus kinase 2 (JAK2) and transcription 3 (STAT3) (induced by LepR), which enhances leptin signaling, were significantly higher and the expression of cytokine signaling-3 (SOCS3), which inhibits leptin signaling, was significantly lower in the two cereal fiber groups than in the HFD group.

Conclusion: Taken together, our findings suggest that cereal fiber can improve leptin resistance and sensitivity by the JAK2/STAT3 pathway in C57BL/6J mice fed a HFD; furthermore, oat fiber is more effective in the improvement of leptin sensitivity than wheat bran fiber, in this murine model.

Keywords: cereal fiber; high-fat/cholesterol diet; leptin resistance; leptin signaling.

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Figures

Fig. 1
Fig. 1
Changes in body weights (a), the food intake (b), and the energy intake (c) of mice in the four diet groups during the whole experiment. Data are means for 12 mice with SD represented by vertical bars. The mean value was significantly different from that of the chow group at *p<0.05, from that of the HFD group at #p<0.05, and from that of the H-oat group at &p<0.05. HFD, high-fat diet; H-oat, high-fat diet supplemented with 0.8% oat fiber; H-wheat, high-fat diet supplemented with 0.8% wheat bran fiber.
Fig. 2
Fig. 2
Changes in the total cholesterol (a) and triglycerides (b) of mice in the four diet groups during the whole experiment. Data are the means for 10~12 mice with SD represented by vertical bars. HFD, high-fat diet; H-oat, high-fat diet supplemented with 0.8% oat fiber; H-wheat, high-fat diet supplemented with 0.8% wheat bran fiber.
Fig. 3
Fig. 3
Changes in the serum leptin (a) and insulin (b) of mice in the four diet groups during the whole experiment. Data are means for 12 mice with SD represented by vertical bars. The mean value was significantly different from that of the Chow group at **p<0.01, and from that of the HFD group at # p<0.05. HFD, high-fat diet; H-oat, high-fat diet supplemented with 0.8% oat fiber; H-wheat, high-fat diet supplemented with 0.8% wheat bran fiber.
Fig. 4
Fig. 4
The relative protein expression of leptin, LepR, JAK2, STAT3, and SOCS3 in the four diet groups. The intensity of the bands was quantified by densitometric analysis and normalized with corresponding β-actin. Data are means for six mice with SD represented by vertical bars. The mean value was significantly different from that of the Chow group at *p<0.05 or **p<0.01, from that of the HFD group at ## p<0.01, and from that of the H-oat group at && p<0.01. HFD, high-fat diet; H-oat, high-fat diet supplemented with 0.8% oat fiber; H-wheat, high-fat diet supplemented with 0.8% wheat bran fiber. HFD, high-fat diet; H-oat, high-fat diet supplemented with 0.8% oat fiber; H-wheat, high-fat diet supplemented with 0.8% wheat bran fiber; LepR, leptin receptor; JAK2, Janus kinase 2; STAT3, transcription 3; SOCS3, cytokine signaling-3.

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