The effect of insulin-induced hypoglycemia on inflammatory markers: A systematic review

•Acute hypoglycaemia induces a pro-inflammatory state.•Elevation of inflammatory markers occurs in both type-1 and non-diabetic subjects.•Activation of the sympathetic nervous system is a likely mediator of these effects. The effects of acute hypoglycemia on markers of inflammation have been investi...

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Published inBrain, behavior, and immunity Vol. 73; pp. 41 - 50
Main Authors Drummond, Juliana B., Barbosa, Izabela G., Dantzer, Robert, Teixeira, Antonio L.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 01.10.2018
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Summary:•Acute hypoglycaemia induces a pro-inflammatory state.•Elevation of inflammatory markers occurs in both type-1 and non-diabetic subjects.•Activation of the sympathetic nervous system is a likely mediator of these effects. The effects of acute hypoglycemia on markers of inflammation have been investigated, but the results have been heterogeneous. We aimed to perform a systematic review about the acute effects of insulin-induced hypoglycemia on inflammatory markers in patients with diabetes as well as non-diabetic subjects. A systematic search of the literature using the electronic databases MEDLINE and SCOPUS was conducted through September 2017. Search terms included: “hypoglycemia”,“ insulin”, “cytokines”, and “inflammation”. We included original studies assessing peripheral inflammatory markers during insulin-induced hypoglycemia in humans. Two hundred twenty-two citations were initially retrieved. Eleven studies were included in our systematic review. Acute hypoglycemia increases total leukocyte number and several pro-inflammatory markers. Elevation in pro-inflammatory markers in response to insulin-induced acute hypoglycemia appears to be of similar magnitude in non-diabetic subjects and in type-1 diabetic patients with intact awareness of hypoglycemia. Adrenaline rises in response to acute hypoglycemia correlates with the increase of pro-inflammatory markers. Acute hypoglycemia induces a pro-inflammatory state in both type-1 diabetic and non-diabetic subjects with no apparent significant difference between these two populations. Activation of the sympathetic nervous system is a likely mediator of these effects.
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ISSN:0889-1591
1090-2139
1090-2139
DOI:10.1016/j.bbi.2018.05.003