Fig 1.
Guar gum protects against dietary-induced obesity.
(A) Body weight evolution was monitored for 12 weeks. (B-C) White adipose tissue to body weight ratio and liver weight to body weight ratio after 12 weeks on diet. (D) Cecal SCFA concentrations were determined by GC/MS after 12 weeks on diet. (E) Cecal mRNA expression of genes involved in SCFA transport was assed via qPCR after 12 weeks on diet. (F) Energy balance was determined by measuring the energy content of the diet and dried homogenized feces after 10 weeks on diet. Uptake is defined as the difference between intake and output. (G-J) Total activity, energy expenditure, VO2 and RER were evaluated using indirect calorimetry data after 10 weeks on diet. Values are presented as mean ± SEM for n = 7–8; *p<0.05, ***p<0.001.
Fig 2.
Guar gum decreases lipogenesis and increases mitochondrial fatty-acid oxidation in liver and adipose tissue.
(A) PPARγ and UCP2 expression in liver and adipose tissue were analyzed by western blot of mice 12 weeks on diet. Quantification is shown in the upper panel. (B-C) After 12 weeks on diet, liver mitochondria were isolated and maximal ADP-stimulated oxygen consumption (i.e. state 3) and resting state oxygen consumption (i.e. state 4) were determined using palmitoyl CoA and malate as substrates. (D) AMP to ATP ratios in liver and adipose tissue were determined by HPLC after 12 weeks on diet. (E) pAMPK, AMPK, pACC, ACC and FASN expression in liver and adipose tissue were analyzed by western blot of mice 12 weeks on diet. Quantification is shown in the right panel. (F) Relative phosphorylation levels were calculated by the ratio of pAMPK/AMPK and pACC/ACC and normalized for control. (G-H) Lipogenesis and ß-oxidation in liver and adipose tissue after 12 weeks of diet. (I-J) Plasma NEFA concentrations and liver triglycerides after 12 weeks of diet. Values are presented as mean ± SEM for n = 6–8; *p<0.05, **p<0.01, ***p<0.001.
Fig 3.
Guar gum increases insulin and glucose sensitivity.
(A-B) Blood glucose and insulin concentrations upon a 4h fast after 12 weeks of diet. (C) HOMA-IR was calculated from fasted glucose and insulin levels after 12 weeks on diet. (D) Insulin tolerance tests were performed on mice for 11 weeks on their respective diets upon a 4h fast. (E) After 11 weeks on their respective diets an intraperitoneal glucose tolerance test was performed in mice that were fasted overnight for 9h. Values are presented as mean ± SEM for n = 6–8; *p<0.05, ***p<0.001.
Fig 4.
Guar gum enhances peripheral glucose handling.
(A) Average blood glucose concentrations during basal and hyperinsulinemic-euglycemic clamps (HIEC) conditions after 12 weeks of diet. (B) Average glucose infusion rates needed to maintain euglycemic conditions. (C-D) Hepatic glucose production and peripheral glucose disposal rate during HIEC conditions. Values are presented as mean ± SEM for n = 6–8; *p<0.05, **p<0.01, ***p<0.001 Guar gum vs. control.
Fig 5.
Guar gum increases colonic GLP-1 expression.
(A) Cecal mRNA expression of PYY and GLP-1 were assessed by qPCR after 12 weeks of diet. (B-C) Plasma PYY and GLP-1 concentrations after 12 weeks of diet. (D) Cecal mRNA expression of Ffar2 was assessed by qPCR after 12 weeks of diet. Values are presented as mean ± SEM for n = 6–8; ***p<0.001.
Fig 6.
Cecal acetate and propionate increase GLP-1 expression.
(A) Cecal SCFA concentrations after 6h cecal SCFA infusion in mice fed HFD without guar gum for 6 weeks. (B) After 6h cecal SCFA infusion cecal mRNA expression of Ffar2, PYY and GLP-1 were assessed qPCR. (C-D) Plasma PYY and GLP-1 concentrations after 6h cecal SCFA infusion. Values are presented as mean ± SEM for n = 6–8; *p<0.05, ***p<0.001.