Abstract
Raised leptin levels have been reported in the placentae and serum of women with elevated blood pressure and proteinuria during pregnancy. The role of leptin in this however remains unknown. This study investigates the effect of leptin administration on systolic blood pressure (SBP) and proteinuria and serum markers of endothelial activation during pregnancy in Sprague Dawley rats. From day 1 of pregnancy, 24 rats were randomised into those given either saline (group 1) or leptin at 60 or 120 μg/kg/body weight/day (groups 2 and 3 resp.). SBP was measured every 5 days and 24-h urinary protein was measured at days 0 and 20 of pregnancy. Animals were euthanised on day 20 of pregnancy, and serum was collected for estimation of E-selectin and ICAM-1. Compared to group 1, SBP during the latter part of the pregnancy was significantly higher in the leptin-treated group (P < 0.01). Urinary protein excretion, serum E-selectin, and ICAM-1 were significantly higher in leptin-treated rats (P < 0.05). It seems that leptin administration to normotensive Sprague Dawley rats during pregnancy significantly increases SBP, urinary protein excretion, and markers of endothelial activation. However, further studies are required to examine the underlying mechanism responsible for this and its relevance to preeclampsia in humans.
Highlights
Leptin, a 16 kDa protein, is primarily secreted from white adipose tissue and plays an important role in controlling food intake and energy balance [1, 2]
No significant differences were seen in water intake and body weight between the groups (Tables 1 and 2)
Compared to the NSP, systolic blood pressure (SBP) was significantly higher on days 15 (LD1-120; P < 0.001) and 20 (LD1-60 and LD1-120; P < 0.001) of pregnancy in the two groups receiving leptin (Figure 1)
Summary
A 16 kDa protein, is primarily secreted from white adipose tissue and plays an important role in controlling food intake and energy balance [1, 2]. Exogenous leptin treatment decreases adiposity by decreasing food intake and increasing energy utilization [3,4,5]. Sympatho-activation following either intra-cerebroventricular or chronic intravenous leptin administration has been shown to increase mean arterial blood pressure and heart rate in rodents [7,8,9]. Agouti mice, which are obese and hyperleptinemic, and transgenic skinny hepatic leptin over-expressing mice have elevated blood pressure [10]. Taken together, these observations demonstrate in several different rodent models that leptin influences blood pressure and that hyperleptinemia in obesity might contribute to the hypertension
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