Aside from a modest benefit in hypertension, renal denervation may also help normalize glucose homeostasis, according to a research group in Germany.
Six months after renal denervation, non-diabetic patients showed better insulin control through their pancreatic beta-cells:
- Fasting glucose was down from 97.1 mg/dL to 92.3 mg/dL (P=0.010)
- Hemoglobin A1c dropped from 5.82% to 5.58% (P=0.008)
- Insulin resistance as assessed by the homeostasis model went from 2.25 down to 1.94 (P=0.004)
C-peptide and insulin became more responsive to glucagon stimulation 6 months after renal denervation as well, reported Roland Schmieder, MD, of Friedrich-Alexander University Erlangen-Nürnberg in Germany, and colleagues in the Dec. 25 issue of the Journal of the American College of Cardiology.
Renal denervation is known to reduce the central sympathetic activity, they noted.
A previous study showed that the most valuable index for predicting functional beta-cell mass was change of C-peptide by glucagon stimulation. Schmieder’s group argued that this is also a valid way to go about measuring the secretory capacity of the beta-cells.
“Notably, we observed a relationship between beta-cell function and reduced fasting glucose 6 months after renal denervation that is predominantly determined by the insulin secretion overnight,” Schmieder’s group wrote.
Their study included 31 consecutive non-diabetic patients with treatment-resistant hypertension (on five antihypertensives on average). The cohort had a mean age of 57.7 years and 67.7% were men. Study participants were split between 22 with normal glucose homeostasis and nine with impaired fasting glucose.
Overall, 24-hour ambulatory blood pressure went from 150 mm Hg to 140 mm Hg at 6 months after renal denervation (P<0.005).
“It is a small, but carefully done study. It shows an effect of renal denervation on sophisticated glycemic parameters. The findings are quite intriguing, especially since the authors states that there were no glucose-lowering drugs utilized, though these provocative results need to be replicated in a larger number of patients in a sham controlled trial,” commented Deepak Bhatt, MD, MPH, of Brigham and Women’s Hospital, who was not involved in the study.
The study was supported by an institutional grant from Medtronic.
Schmieder disclosed research funding and advising/speaking for Medtronic.
Bhatt reported research funding from Abbott, Amarin, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Chiesi, Eisai, Ethicon, Forest Laboratories, Idorsia, Ironwood, Ischemix, Lilly, Medtronic, PhaseBio, Pfizer, Regeneron, Roche, Sanofi Aventis, Synaptic, and The Medicines Company