Abstract: PO1823
The Role of Ketogenic Diet on the Development of Salt-Sensitive Hypertension
Session Information
- Hypertension and CVD: Mechanisms
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1403 Hypertension and CVD: Mechanisms
Authors
- Golosova, Daria, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
- Kravtsova, Olha, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
- Levchenko, Vladislav, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
- Staruschenko, Alexander, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
Background
Hypertension is one of the most important risk factors for cardiovascular disease, which is the leading cause of mortality in the US. Two-thirds of hypertension cases are positively correlated with excessive weight gain. The ketogenic diet (KD) may be useful as part of the treatment of cardiovascular complications especially in obese patients. The KD, a low-carb high-fat diet, triggering the body to burn fat for energy instead of carbohydrates, has gained popularity through the weight loss community. We hypothesized that KD can have protective effects during the development of salt-induced hypertension.
Methods
The Dahl salt-sensitive (SS) rats fed a high salt diet develop hypertension accompanied by kidney injury. The Dahl SS rats were given either 4% NaCl diet (HS; Dyets Inc, 113756) or 4% NaCl modified KD (Harland Tekland, TD 190564) with free access to water for 5 weeks. Blood pressure was monitored with telemetry throughout the study, and urine samples were collected in metabolic cages on days 0, 7, 14, 28, and 35. At the end of the protocol animals were sacrificed and blood and kidney tissues were harvested for the analyses.
Results
Dahl SS rats fed a KD had a lower blood pressure compared to control rats fed a HS diet. Mean arterial pressure was 147 ± 5 mmHg vs 179 ± 9 mmHg (KD vs HS, p<0.05). Reduced renal hypertrophy with decreased kidney to body weight ratio (1.00 ± 0.06 vs 1.25 ± 0.04, p<0.05 compared to HS) and smaller kidneys (3.5 ± 0.1 vs 4.5 ± 0.2 g, p<0.05 compared to HS) were found in the KD group. No differences in glomerular damage scores were detected between the groups. The rats on KD experienced hypoglycemia (282 ± 9 vs 335 ± 14 mg/dL, p<0.05 compared to HS) with reduced glucose urinary excretion (5 ± 1 vs 32 ± 7, glucose to creatinine ratio, p<0.05 compared to HS). Microbiome analyses revealed an increase in the relative abundance of putatively beneficial gut microbiota (Lactobacillus) and a reduced level of putatively pro-inflammatory taxa (Turicibacter).
Conclusion
Therefore, prolonged KD intervention provides a protective effect on the development of SS hypertension. Our data revealed that KD during HS challenge resulted in decreased blood pressure, reduced kidney hypertrophy, and diminished levels of plasma glucose.
Funding
- NIDDK Support