Summary 1. Overconsumption of fructose produces glucose intolerance, autonomic abnormalities and renal dysfunction and may be related to the worldwide epidemic of obesity and diabetes. 2. Experiments were conducted to determine whether the time period (light or dark) of fructose consumption influenced the pathological consequences. C57BL mice were given standard chow and assigned to one of three groups: (i) control (n = 10), which received water over a 24 h period; (ii) FL (n = 11), which received 10% fructose solution during the 12 h light period; and (iii) FD (n = 11), which received 10% fructose solution during the 12 h dark period. 3. There was a time related increase in body weight for all groups (P < 0.01, 2 vs 6 wks). There was a greater increase in body fat in the FL group compared with the control and FD groups. The changes in adiposity occurred even though the total caloric intake was not significantly different among the groups (approximately 18 kcal/day). Total fluid (water + fructose) consumption was greater in the FD and FL groups compared with control at 6 weeks. Significant increases were noted for plasma insulin and leptin at 8 weeks, with highest levels in the FL compared with FD group (P < 0.05). There were no significant changes in glucose, glucose tolerance, cholesterol, triglycerides or adiponectin. 4. The results of the present study suggest that there is a mismatch in caloric consumption, metabolism and adiposity as related to the light–dark cycle of fructose consumption. These findings have clinical implications in the control of bodyweight, abdominal fat accumulation and Type 2 diabetes.

Data suggest that early exposure to high fructose intake produced marked alterations in metabolic and cardiovascular function. When stimulated by NaCl, the fructose-fed subjects showed further impairment in cardiac function.

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Beta‐adrenoceptors (β‐AR) play an important role in cardiac autonomic function. There are three β‐AR subtypes (β(1), β(2), β(3)) described and identified. β(3) when stimulated, induce negative inotropic effects in order to protect the heart from catecholamine overstimulation. The aim of this study was to determine the cardiac autonomic modulation in experimental model of β3 adrenergic receptor absence. Knockout and wild type mice for β3 receptor were used (ARβ3KO and WT, respectively). The male animals with 8 weeks old were submitted to catheterization of carotid artery. This catheter was connected to a transducer and continuous signals of blood pressure (BP) and heart rate (HR) were recorded and analyzed by Windaq® software. The variability of resultant signal was evaluated in time and frequency domain by Fourier Fast Transform. Although there were no difference in BP and HR between the groups, the HR and BP variance are respectively 113% and 96% higher on ARβ3KO. Moreover, the LF component for HR (24.62 ± 3.4 vs. 7.90 ± 1.8 ms²) and BP (38.04 ± 8.1vs. 20.32 ± 2.8 mmHg²) were increased in ARβ3KO when compared with WT. The sympathetic‐vagal balance was increased in ARβ3KO (1.58 ± 0.28) when compared to WT (0.61 ± 0.09). In conclusion, our data showed that the absence of β3 receptor determined an increase in cardiac sympathetic modulation confirming the cardioprotective role this receptors.