Table 1.
Sequences of the primers used in real-time PCR.
Figure 1.
Fruit picture and HPLC chromatograms of major flavonoids of FME.
(A) Fruit picture. (B) Chromatograms of standards: (1) neoeriocitrin; (2) narirutin; (3) naringin; (4) hesperidin; (5) neohesperidin; (6) poncirin; (7) naringenin. (C) The major flavonoids of FME were determined by comparing with the chromatogram of standards. (1) neoeriocitrin; (6) poncirin.
Figure 2.
FME blocked the high-fat diet-fed obesity and hyperglycemia in C57BL/6 mice in the preventive treatment.
(A): Body weight change. (B): Food intake amount. (C): Fasting blood glucose levels. (D): Intraperitoneal glucose tolerance test (GTT). (E): The area under the curve (AUC) during GTT. (F): White adipocyte areas. (G): H&E staining (×200) of WAT. Values are presented as mean ± SEM (n = 7). Values with different letters were significantly different (p<0.05).
Figure 3.
FME decreases serum lipid levels in C57BL/6 mice in the preventive treatment.
(A): Total cholesterol. (B): Serum triglyceride. (C): High-density lipoprotein cholesterol. (D): Low-density lipoprotein cholesterol. Values are presented as mean ± SEM (n = 7). Values with different letters were significantly different (p<0.05).
Figure 4.
FME improves hyperglycemia in obese C57 BL/6 mice in therapeutic treatment.
(A) Body weights before and after treatment. (B) Food intake amount. (C) Intraperitoneal glucose tolerance test (GTT). (D) The area under the curve (AUC) during GTT. (E) Intraperitoneal insulin tolerance test (ITT). (F) The area under the curve (AUC) during ITT. Values are expressed as means ± SEM (n = 7). Values with different letters were significantly different (p<0.05).
Figure 5.
FME improves lipid profile in obese C57 BL/6 mice in the therapeutic treatment.
(A): Total cholesterol. (B): Serum triglyceride. (C): High-density lipoprotein cholesterol. (D): Low-density lipoprotein cholesterol. Values are presented as mean ± SEM (n = 7). Values with different letters were significantly different (p<0.05).
Figure 6.
FME improves lipid accumulation in the liver of C57BL/6 mice induced by high-fat diet.
(A): Triglyceride contents in the liver of preventive treatment. (B): Total cholesterol contents in the liver of preventive treatment. (C): Triglyceride contents in the liver of therapeutic treatment. (D): Total cholesterol contents in the liver of therapeutic treatment. Values are presented as mean ± SEM (n = 7). Values with different letters were significantly different (p<0.05).
Figure 7.
FME influences the expression of PPARα and its target genes in vivo.
(A): The relative gene expression levels of PPARα and its target genes in the liver of FME-treated and HF-fed mice in the therapeutic treatment. β-actin was used as an internal control. (B): The relative gene expression levels of UCP1, UCP2 and UCP3 in the brown adipose tissue of FME-treated and HF-fed mice in the therapeutic treatment. Values are presented as mean ± SEM (n = 6). Values with different letters were significantly different (p<0.05).