Distinct Impact of Natural Sugars from Fruit Juices and Added Sugars on Caloric Intake, Body Weight, Glycaemia, Oxidative Stress and Glycation in Diabetic Rats

Abstract

Although fruit juices are a natural source of sugars, there is a controversy whether their sugar content has similar harmful effects as beverages' added-sugars. We aimed to study the role of fruit juice sugars in inducing overweight, hyperglycaemia, glycation and oxidative stress in normal and diabetic animal models. In diabetic Goto-Kakizaki (GK) rats, we compared the effects of four different fruit juices (4-weeks) with sugary solutions having a similar sugar profile and concentration. In vitro, the sugary solutions were more susceptible to AGE formation than fruit juices, also causing higher postprandial glycaemia and lower erythrocytes' antioxidant capacity in vivo (single intake). In GK rats, ad libitum fruit juice consumption (4-weeks) did not change body weight, glycaemia, oxidative stress nor glycation. Consumption of a matched volume of sugary solutions aggravated fasting glycaemia but had a moderate impact on caloric intake and oxidative stress/glycation markers in tissues of diabetic rats. Ad libitum availability of the same sugary solutions impaired energy balance regulation, leading to higher caloric intake than ad libitum fruit juices and controls, as well as weight gain, fasting hyperglycaemia, insulin intolerance and impaired oxidative stress/glycation markers in several tissues. We demonstrated the distinct role of sugars naturally present in fruit juices and added sugars in energy balance regulation, impairing oxidative stress, glycation and glucose metabolism in an animal model of type 2 diabetes.

Keywords: fruit juices; glycation; hyperglycaemia; natural and added sugars; oxidative stress.

Figure 1

The AGEs CML, MG-H1 and Argpyrimidine were detected by dot blot (A) in fruit juices and sugary solutions with the same sugars profile (B) in the presence or absence of BSA, at 4 °C or 37 °C. In other to determine the postprandial glycaemia, an OGTT was performed (C) and glycaemia and total antioxidant capacity of erythrocytes was determined after intake of 4 mL of red fruits (D,H), orange (E,I), peach (F,J) and pear (G,K) fruit juices or a sugary solution with the equivalent sugars profile. * different from Water; # different from the fruit juice. 1 symbol, p < 0.05; 3 symbols, p < 0.001.

Figure 2

Normal and diabetic rats were treated for 4 weeks with fruit juices ad libitum. Diabetic rats were also treated during the same period with a matched sugary solution in the same volume (GK_S) or ad libitum (GK_S_AL) (A). Body weight was monitored during the experimental period (B–E) and weight gain calculated at each time-point (F–I). Food intake (J–M) and consumption of water/juice/sugary solution (N–Q) were monitored throughout all the experimental period. The total caloric intake/day was calculated (R–U). * different from Wistar; # different from GK; $ different from GK_Juice. & Different from GK_Juice_S. 1 symbol, p < 0.05; 2 symbols, p < 0.01; 3 symbols, p < 0.001.

Figure 2

Normal and diabetic rats were treated for 4 weeks with fruit juices ad libitum. Diabetic rats were also treated during the same period with a matched sugary solution in the same volume (GK_S) or ad libitum (GK_S_AL) (A). Body weight was monitored during the experimental period (B–E) and weight gain calculated at each time-point (F–I). Food intake (J–M) and consumption of water/juice/sugary solution (N–Q) were monitored throughout all the experimental period. The total caloric intake/day was calculated (R–U). * different from Wistar; # different from GK; $ different from GK_Juice. & Different from GK_Juice_S. 1 symbol, p < 0.05; 2 symbols, p < 0.01; 3 symbols, p < 0.001.

Figure 3

Fasting (6 h) glycaemia was evaluated weekly and calculated the percentage of the initial value (A–D). Fasting glycaemia at the end of the treatment is shown in (E–H). Before and after the experimental period an i.p. insulin tolerance test was performed and the area under the curve was calculated (I–L). * different from Wistar; # different from GK; $ different from GK_Juice. 1 symbol, p < 0.05; 2 symbols, p < 0.01; 3 symbols, p < 0.001.

Figure 4

In isolated erythrocytes, total antioxidant capacity was determined (A–D) and CML (E–H) and argpyrimidine (I–L) were detected by dot blot. * different from Wistar. 1 symbol, p < 0.05; 2 symbols, p < 0.01.

Figure 5

Liver weight was recorded (A–D) and the levels of catalase were determined by Western Blot (E–H). Representative western blot membranes of GLO-1 and dot blot membranes of CML and argpyrimidine in the liver are shown in (I). * different from Wistar; # different from GK; $ different from GK_Juice; & different from GK_S. 1 symbol, p < 0.05; 2 symbols, p < 0.01; 3 symbols, p < 0.001.

Figure 6

Epididymal adipose tissue weight was recorded (A–D) and the levels of catalase (E–H) and GLO-1 (I–L) in the tissue were determined by Western Blot. Representative dot blot membranes of CML and argpyrimidine in the adipose tissue are shown in (M). * different from Wistar. 1 symbol, p < 0.05; 2 symbols, p < 0.01.

Figure 7

Heart weight was recorded (A–D) and the levels of catalase were determined by Western blot (E–H). Representative western blot membranes of GLO-1 in the heart are shown in (I). Heart CML (J–M) and argpyrimidine (N–Q) were determined by dot blot. 8-Isoprostane levels were determined as a marker of lipid peroxidation (R–U). * different from Wistar; # different from GK; $ different from GK_Juice. 1 symbol, p < 0.05; 2 symbols, p < 0.01.

Figure 7

Heart weight was recorded (A–D) and the levels of catalase were determined by Western blot (E–H). Representative western blot membranes of GLO-1 in the heart are shown in (I). Heart CML (J–M) and argpyrimidine (N–Q) were determined by dot blot. 8-Isoprostane levels were determined as a marker of lipid peroxidation (R–U). * different from Wistar; # different from GK; $ different from GK_Juice. 1 symbol, p < 0.05; 2 symbols, p < 0.01.

Figure 8

Kidney weight was recorded (A–D). Representative Western blot membranes of catalase and GLO-1 and dot blot membranes of CML in the kidney are shown in (E). Kidney argpyrimidine was determined by dot blot (F–I). * different from Wistar; # different from GK; $ different from GK_Juice; & different from GK_S. 1 symbol, p < 0.05; 2 symbols, p < 0.01.

Figure 9

Detection of the dihydroethidium (DHE) probe for superoxide anion determination. (A) shows the negative control (no probe). Representative images of the glomeruli are shown for control Wistar rats (B), Wistar rats maintained with ad libitum access to fruit juices (C), control GK rats (D), GK rats maintained with ad libitum access to fruit juices (E), GK rats treated with respective sugary solutions matched in sugar profile, concentration and quantity (F), and GK rats maintained with ad libitum access to the same sugary solutions (G). (H–K) show the quantification of glomerular DHE staining for the different experimental conditions of each sample tested. # different from GK. 1 symbol, p < 0.05; 2 symbols, p < 0.01.