Vol 4, No 2 (2000)
Original paper
Published online: 2000-05-23
Do Leptin and Norepinephrine Influence Hypertension in Obese Individuals?
Nadciśnienie tętnicze 2000;4(2):89-96.
Abstract
Background: Obesity is commonly associated with hypertension, diabetes type 2, dyslipidaemia and other components of polymetabolic syndrome. There are several factors influencing the development of obesity, the activity of sympathetic nervous system belongs to the most important. Leptin, the newly discovered hormone, produced by adipose tissue, responsible for regulation of food intake, plays role also in the regulation of cardiovascular system and blood pressure. The aim of the study was an attempt of answering the question whether and in what degree obese subjects differ from obese hypertensives due to metabolic parameters, including leptinaemia and norepinephrinaemia, and whether those hormones play their role in forming hypertension in those patients.
Methods: We examined 30 obese patients with mild to moderate hypertension — group 1 (17F:13M, mean age 49,0 ± ± 8,13) and 25 obese patients without hypertension — group 2 (15F:10M, mean age 46,7 ± 9,81). We measured BMI, WHR and amounts of relative (% FAT) and absolute (kg FAT) adipose tissue by the bioimpedance analysis. We also measured the following fasting parameters: glycaemia, insulinaemia, leptinaemia, lipidaemia, concentrations of norepinephrine. Insulin resistance was counted as a quotient of fasting insulinaemia to glycaemia (IRI/G).
Results: We found significantly higher values of WHR, insulinaemia, IRI/G, leptinaemia (border-line significance), concentrations of total cholesterol and LDL-cholesterol in group 1. We found several positive correlations in group 1: between leptin and BMI (p < 0,05; r = 0,75), WHR (p < 0,02; r = 0,40), kg FAT (p < 0,001; r = 0,71), % FAT (p < 0,007; r = 0,49), DBP (p < 0,05; r = 0,41), HR (p < 0,05; r = 0,35), insulinaemia (p < 0,05; r = 0,35), IRI/G (p < 0,05, r = 0,39).We also found negative correlation between plasma leptin and norepinephrine (p < 0,05; r = –0,60) in this group. In the group with isolated obesity (group 2) we found the following positive correlations: between leptin and BMI (p < 0,05; r = 0,74), kg FAT (p < 0,001; r = 0,45), % FAT (p < 0,005; r = 0,45), HR (p < 0,05; r = 0,36). The negative correlation was found between plasma leptin and norepinephrine (p < 0,05; r = –0,66).
Conclusions: 1. Concentrations of norepinephrine and heart rate were within the normal ranges and did not differ significantly in both analyzed groups. 2. Positive correlation between leptin and diastolic blood pressure, heart rate, insulinaemia, WHR in obese hypertensives is consistent with the hypothesis suggesting the role of leptin in the development of primary hypertension. 3. The negative correlation between leptin and norepinephrine concentrations in hyperleptinaemic subjects suggests that decreased activity of sympathetic nervous system may explain the development of obesity.
Methods: We examined 30 obese patients with mild to moderate hypertension — group 1 (17F:13M, mean age 49,0 ± ± 8,13) and 25 obese patients without hypertension — group 2 (15F:10M, mean age 46,7 ± 9,81). We measured BMI, WHR and amounts of relative (% FAT) and absolute (kg FAT) adipose tissue by the bioimpedance analysis. We also measured the following fasting parameters: glycaemia, insulinaemia, leptinaemia, lipidaemia, concentrations of norepinephrine. Insulin resistance was counted as a quotient of fasting insulinaemia to glycaemia (IRI/G).
Results: We found significantly higher values of WHR, insulinaemia, IRI/G, leptinaemia (border-line significance), concentrations of total cholesterol and LDL-cholesterol in group 1. We found several positive correlations in group 1: between leptin and BMI (p < 0,05; r = 0,75), WHR (p < 0,02; r = 0,40), kg FAT (p < 0,001; r = 0,71), % FAT (p < 0,007; r = 0,49), DBP (p < 0,05; r = 0,41), HR (p < 0,05; r = 0,35), insulinaemia (p < 0,05; r = 0,35), IRI/G (p < 0,05, r = 0,39).We also found negative correlation between plasma leptin and norepinephrine (p < 0,05; r = –0,60) in this group. In the group with isolated obesity (group 2) we found the following positive correlations: between leptin and BMI (p < 0,05; r = 0,74), kg FAT (p < 0,001; r = 0,45), % FAT (p < 0,005; r = 0,45), HR (p < 0,05; r = 0,36). The negative correlation was found between plasma leptin and norepinephrine (p < 0,05; r = –0,66).
Conclusions: 1. Concentrations of norepinephrine and heart rate were within the normal ranges and did not differ significantly in both analyzed groups. 2. Positive correlation between leptin and diastolic blood pressure, heart rate, insulinaemia, WHR in obese hypertensives is consistent with the hypothesis suggesting the role of leptin in the development of primary hypertension. 3. The negative correlation between leptin and norepinephrine concentrations in hyperleptinaemic subjects suggests that decreased activity of sympathetic nervous system may explain the development of obesity.
Keywords: leptinnorepinephrineobesityhypertensionsympathetic nervous system