TY - JOUR
T1 - Effect of insulin-induced hypoglycaemia on the peripheral nervous system
T2 - focus on adaptive mechanisms, pathogenesis and histopathological changes
AU - Jensen, Vivi Flou Hjorth
AU - Mølck, A.-M.
AU - Bøgh, I. B.
AU - Lykkesfeldt, Jens
N1 - © 2014 British Society for Neuroendocrinology.
PY - 2014/8
Y1 - 2014/8
N2 - Insulin-induced hypoglycaemia (IIH) is a common acute side effect in type 1 and type 2 diabetic patients, especially during intensive insulin therapy. The peripheral nervous system (PNS) depends on glucose as its primary energy source during normoglycaemia and, consequently, it may be particularly susceptible to IIH damage. Possible mechanisms for adaption of the PNS to IIH include increased glucose uptake, utilisation of alternative energy substrates and the use of Schwann cell glycogen as a local glucose reserve. However, these potential adaptive mechanisms become insufficient when the hypoglycaemic state exceeds a certain level of severity and duration, resulting in a sensory-motor neuropathy with associated skeletal muscle atrophy. Large myelinated motor fibres appear to be particularly vulnerable. Thus, although the PNS is not an obligate glucose consumer, as is the brain, it appears to be more prone to IIH than the central nervous system when hypoglycaemia is not severe (blood glucose level ≤ 2 mm), possibly reflecting a preferential protection of the brain during periods of inadequate glucose availability. With a primary focus on evidence from experimental animal studies investigating nondiabetic IIH, the present review discusses the effect of IIH on the PNS with a focus on adaptive mechanisms, pathogenesis and histological changes.
AB - Insulin-induced hypoglycaemia (IIH) is a common acute side effect in type 1 and type 2 diabetic patients, especially during intensive insulin therapy. The peripheral nervous system (PNS) depends on glucose as its primary energy source during normoglycaemia and, consequently, it may be particularly susceptible to IIH damage. Possible mechanisms for adaption of the PNS to IIH include increased glucose uptake, utilisation of alternative energy substrates and the use of Schwann cell glycogen as a local glucose reserve. However, these potential adaptive mechanisms become insufficient when the hypoglycaemic state exceeds a certain level of severity and duration, resulting in a sensory-motor neuropathy with associated skeletal muscle atrophy. Large myelinated motor fibres appear to be particularly vulnerable. Thus, although the PNS is not an obligate glucose consumer, as is the brain, it appears to be more prone to IIH than the central nervous system when hypoglycaemia is not severe (blood glucose level ≤ 2 mm), possibly reflecting a preferential protection of the brain during periods of inadequate glucose availability. With a primary focus on evidence from experimental animal studies investigating nondiabetic IIH, the present review discusses the effect of IIH on the PNS with a focus on adaptive mechanisms, pathogenesis and histological changes.
KW - Faculty of Health and Medical Sciences
KW - Insulin
KW - Hypoglycaemia
KW - glucose transporters
KW - peripheral neuropathy
KW - axonal degeneration
KW - skeletal muscle atrophy
U2 - 10.1111/jne.12170
DO - 10.1111/jne.12170
M3 - Journal article
C2 - 24921897
SN - 0953-8194
VL - 26
SP - 482
EP - 496
JO - Journal of Neuroendocrinology
JF - Journal of Neuroendocrinology
IS - 8
ER -
