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Träfflista för sökning "WFRF:(Benrick Anna 1979 ) ;pers:(Protto V.)"

Sökning: WFRF:(Benrick Anna 1979 ) > Protto V.

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1.
  • Benrick, Anna, 1979, et al. (författare)
  • Autonomic nervous system activation mediates the increase in whole-body glucose uptake in response to electroacupuncture
  • 2017
  • Ingår i: Faseb Journal. - : Federation of American Societies for Experimental Biology. - 0892-6638 .- 1530-6860. ; 31:8, s. 3288-3297
  • Tidskriftsartikel (refereegranskat)abstract
    • A single bout of low-frequency electroacupuncture (EA) causing muscle contractions increases whole-body glucose uptake in insulin-resistant rats. We explored the underlying mechanism of this finding and whether it can be translated into clinical settings. Changes in glucose infusion rate (GIR) were measured by euglycemic-hyperinsulinemic clamp during and after 45 min of low-frequency EA in 21 overweight/obese women with polycystic ovary syndrome (PCOS) and 21 controls matched for age, weight, and body mass index (experiment 1) and in rats receiving autonomic receptor blockers (experiment 2). GIR was higher after EA in controls and women with PCOS. Plasma serotonin levels and homovanillic acid, markers of vagal activity, decreased in both controls and patients with PCOS. Adipose tissue expression of pro-nerve growth factor (proNGF) decreased, and the mature NGF/proNGF ratio increased after EA in PCOS, but not in controls, suggesting increased sympathetic-driven adipose tissue metabolism. Administration of alpha-/beta-adrenergic receptor blockers in rats blocked the increase in GIR in response to EA. Muscarinic and dopamine receptor antagonist also blocked the response but with slower onset. In conclusion, a single bout of EA increases whole-body glucose uptake by activation of the sympathetic and partly the parasympathetic nervous systems, which could have important clinical implications for the treatment of insulin resistance.
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2.
  • Stener-Victorin, Elisabet, 1964, et al. (författare)
  • Changes in HbA(1c) and circulating and adipose tissue androgen levels in overweight-obese women with polycystic ovary syndrome in response to electroacupuncture
  • 2016
  • Ingår i: Obesity Science & Practice. - : Wiley. - 2055-2238. ; 2:4, s. 426-435
  • Tidskriftsartikel (refereegranskat)abstract
    • Aim Insulin sensitivity is similar to 40% lower in women with polycystic ovary syndrome (PCOS) than in controls. We tested the hypothesis that 5 weeks of electroacupuncture treatment improves glucose regulation and androgen levels in overweight/obese women with PCOS. Seventeen women with PCOS, aged 18 to 38years, with a body mass index (BMI) >= 25 kg/m(2) and diagnosed with PCOS were included in this experimental and feasibility study and subjected to five weeks of electroacupuncture treatments three times/week. The primary outcome was changes in whole-body glucose homeostasis measured by euglycemic hyperinsulinemic clamp before and after the intervention. Secondary outcome were changes in HbA(1c), circulating catecholamines, adipocyte size and adipose tissue expression of sex steroids and nerve growth factor (NGF). No significant change in glucose homeostasis was observed, but HbA(1c) decreased by 9.5% (p=0.004), circulating testosterone decreased by 22% (p=0.0007) and dihydrotestosterone decreased by 12% (p=0.007). The two vagal activity markers of plasma serotonin levels and the dopamine metabolite homovanillic acid decreased by 21% (p=0.027) and 20% (p=0.011), respectively. Adipose tissue concentrations of testosterone decreased by 18% (p=0.049), and androstenedione decreased by 13% (p=0.035), and mature NGF/proNGF ratio, a marker of sympathetic activity, increased (p=0.04). These changes occurred without changes in anthropometrics. Five weeks of electroacupuncture treatment improves HbA(1c) and circulating and adipose tissue androgens in women with PCOS. This effect is mediated, at least in part, via modulation of vagal activity and adipose tissue sympathetic activity. Based on these findings, we have recently initiated a randomized controlled study (NTC02647827).
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