The impact of sugar-sweetened beverage intake on rat cardiac function

Abstract

Aims: Although there is evidence linking sugar-sweetened beverage (SSB) intake with the development of cardio-metabolic diseases, the underlying mechanisms remain unclear. The current study therefore evaluated the effects of SSB consumption by establishing a unique in-house in vivo experimental model.

Main methods: Male Wistar rats were divided into two groups: a) one consuming a popular local SSB (SSB- Jive), and b) a control group (Control-water) for a period of three and six months (n = 6 per group), respectively. Rats were gavaged on a daily basis with an experimental dosage amounting to half a glass per day (in human terms) (SSB vs. water). Cardiac function was assessed at baseline (echocardiography) and following ex vivo ischemia-reperfusion of the isolated perfused working rat heart. Oral glucose tolerance tests and mitochondrial respiratory analyses were also performed. In addition, the role of non-oxidative glucose pathways (NOGPs), i.e. the polyol pathway, hexosamine biosynthetic pathway (HBP) and PKC were assessed.

Key findings: These data show that SSB intake: a) resulted in increased weight gain, but did not elicit major effects in terms of insulin resistance and cardiac function after three and six months, respectively; b) triggered myocardial NOGP activation after three months with a reversion after six months; and c) resulted in some impairment in mitochondrial respiratory capacity in response to fatty acid substrate supply after six months.

Significance: SSB intake did not result in cardiac dysfunction or insulin resistance. However, early changes at the molecular level may increase risk in the longer term.

Keywords: Biochemistry; Cardiology; Molecular biology; Nutrition; Physiology.

Fig. 1

The impact of SSB consumption on weight gain. A) three months, and B) six months. The area under the curve was calculated at the C) 3 months and D) 6 months, time points. The animals were weighed on a weekly basis, and weight gained by each rat was then compared to its own baseline weight as a percentage Results are displayed as mean ± SEM. For all groups n = 6. **P < 0.01.

Fig. 2

The effects of SSB consumption - oral glucose tolerance tests. A) OGTT - three months, B) OGTT - six months, C) AUC - 3 months, and D) AUC – 6 months. OGTTs were performed biweekly to monitor the animal's glycemic states and to evaluate the effects of SSB on postprandial hyperglycemic excursions. Glucose levels were tested at 0, 5, 10, 15, 30, 45, 60 and 120 minutes (n = 12 for baseline [week 1] to three months; n = 6 for the six -month time point). Values are expressed as mean ± SEM. Significantly different compared to Control group: **P < 0.005 and ***P < 0.001.

Fig. 3

SSB intake and effects on mitochondrial respiratory function. A) – D) glycolytic substrates, and E) – H) FA substrates. A- LEAK, B- OXPHOS, C- ETS capacity and D- excess E-R. The substrates used for these experiments included pyruvate (P), glutamate (G) and malate (M). E- LEAK, F- OXPHOS, G- ETS capacity and H- excess E-R. The substrates used for these experiments included octanoyl carnitine (Oct) and malate (M). A total number of n = 6 was used for all groups. Results are displayed as mean ± SEM and significance is shown as *P < 0.01 compared to Control.

Fig. 4

(part 1): The impact of SSB consumption on heart function (ex vivo Langendorff perfusions). Perfusion data, A, C, E), 3 months, B, D, F) 6 months. Cardiac output (QC) was calculated as the sum of aortic output (QA) and coronary flow (CO). The aortic systolic and diastolic pressure (mmHg) and HR [beats per minute (bpm)] were monitored and recorded on a computerized system through a side-arm of the aortic cannula, and total work performance was calculated as follows: pressure power + kinetic power = Watt. Results are displayed as mean ± SEM. A final n = 8 for all groups were used. (part 2): The impact of SSB consumption on heart function (ex vivo Langendorff perfusions). Perfusion data, G, I, K), 3 months, H, J, L) 6 months. The aortic systolic and diastolic pressure (mmHg) and HR [beats per minute (bpm)] were monitored and recorded on a computerized system through a side-arm of the aortic cannula connected to a Viggo-Spectramed pressure transducer coupled to the computer system. Total work performance was calculated as follows: pressure power + kinetic power = Watt. A final n = 8 for all groups were used.

Fig. 5

The effects of SSB intake on infarct size. Infarct size and area at risk, A&C), 3 months, B&D) 6 months (n = 8). Infarct size is expressed as the percentage of the area at risk (I/AR%). Results are displayed as mean ± SEM and significance is shown as *P < 0.05 compared to Control.

Fig. 6

Markers of myocardial glucose and lipid metabolism following SSB intake. A, C and E is 3 Months and B, D and F represents 6 months. A and B show myocardial triglyceride stores with SSB consumption. C and D represent glycogen stores measured in the rat heart. E and F depict glycogen synthesis (n = 6 for all groups). Data are displayed as mean ± SEM and significance between the groups is displayed as *P < 0.05.

Fig. 7

NOGP regulation following SSB intake. NOGPs, A, C & E) 3 months, B, D & F) 6 months (n = 6). Values are expressed as mean ± SEM and significance is shown as **P < 0.01.

Fig. 8

Summary of findings of SSB-mediated effects. A) three months and B) six months. SSB- sugar-sweetened beverage, AMI- acute myocardial infarction, NOGP- Non-oxidative glucose pathways, HBP- Hexosamine biosynthetic pathway.