Altered hormonal and autonomic nerve responses to hypo- and hyperglycaemia are found in overweight and insulin-resistant individuals and may contribute to the development of type 2 diabetes

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Lundqvist, Martin H.Uppsala universitet,Klinisk diabetologi och metabolism (author)

Altered hormonal and autonomic nerve responses to hypo- and hyperglycaemia are found in overweight and insulin-resistant individuals and may contribute to the development of type 2 diabetes

Article/chapterEnglish2021

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2020-11-26
Springer,2021
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LIBRIS-ID:oai:DiVA.org:umu-177495
https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-177495URI
https://doi.org/10.1007/s00125-020-05332-zDOI
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-430272URI

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Language:English
Summary in:English

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Aims/hypothesis: Results from animal models and some clinical work suggest a role for the central nervous system (CNS) in glucose regulation and type 2 diabetes pathogenesis by modulation of glucoregulatory hormones and the autonomic nervous system (ANS). The aim of this study was to characterise the neuroendocrine response to various glucose concentrations in overweight and insulin-resistant individuals compared with lean individuals.Methods: Overweight/obese (HI, n = 15, BMI ≥27.0 kg/m2) and lean (LO, n = 15, BMI <27.0 kg/m2) individuals without diabetes underwent hyperinsulinaemic euglycaemic–hypoglycaemic clamps and hyperglycaemic clamps on two separate occasions with measurements of hormones, Edinburgh Hypoglycaemic Symptom Scale (ESS) score and heart rate variability (HRV). Statistical methods included groupwise comparisons with Mann–Whitney U tests, multilinear regressions and linear mixed models between neuroendocrine responses and continuous metabolic variables.Results: During hypoglycaemic clamps, there was an elevated cortisol response in HI vs LO (median ΔAUC 12,383 vs 4793 nmol/l × min; p = 0.050) and a significantly elevated adrenocorticotropic hormone (ACTH) response in HI vs LO (median ΔAUC 437.3 vs 162.0 nmol/l × min; p = 0.021). When adjusting for clamp glucose levels, obesity (p = 0.033) and insulin resistance (p = 0.009) were associated with elevated glucagon levels. By contrast, parasympathetic activity was less suppressed in overweight individuals at the last stage of hypoglycaemia compared with euglycaemia (high-frequency power of HRV, p = 0.024). M value was the strongest predictor for the ACTH and PHF responses, independent of BMI and other variables. There was a BMI-independent association between the cortisol response and ESS score response (p = 0.024). During hyperglycaemic clamps, overweight individuals displayed less suppression of glucagon levels (median ΔAUC −63.4% vs −73.0%; p = 0.010) and more suppression of sympathetic relative to parasympathetic activity (low-frequency/high-frequency power, p = 0.011).Conclusions/interpretation: This study supports the hypothesis that altered responses of insulin-antagonistic hormones and the ANS to glucose fluctuations occur in overweight and insulin-resistant individuals, and that these responses are probably partly mediated by the CNS. Their potential role in development of type 2 diabetes needs to be addressed in future research.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Endokrinologi och diabetes hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine Endocrinology and Diabetes hsv//eng
ACTH
Central nervous system
Cortisol
Diabetes
Glucoregulatory hormones
Glucose
Insulin resistance
Obesity

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Almby, Kristina E.Uppsala universitet,Klinisk diabetologi och metabolism(Swepub:uu)krial435 (author)
Wiklund, UrbanUmeå universitet,Radiofysik,Department of Radiation Sciences, Biomedical Engineering, Umeå University, Umeå, Sweden(Swepub:umu)urwi0001 (author)
Abrahamsson, Niclas,1976-Uppsala universitet,Klinisk diabetologi och metabolism(Swepub:uu)nicab972 (author)
Kamble, Prasad G.Uppsala universitet,Klinisk diabetologi och metabolism(Swepub:uu)kampr247 (author)
Pereira, Maria J.,1981-Uppsala universitet,Klinisk diabetologi och metabolism(Swepub:uu)marpe927 (author)
Eriksson, JanUppsala universitet,Klinisk diabetologi och metabolism(Swepub:uu)janer909 (author)
Uppsala universitetKlinisk diabetologi och metabolism (creator_code:org_t)

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In:Diabetologia: Springer64:3, s. 641-6550012-186X1432-0428

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