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Le glutamate augmente le rebond glucidique

03/10/2015 | Etudes Compléments alimentaires et Etudes Perte de poids


Le glutamate augmente le rebond glucidique sans agir comme booster d’insuline

Glutamate increased glucose uptake in l6 myotubes in a concentration- and time-dependent manner that is mediated
Appl. Physiol. Nutr. Metab. Vol. 40, 2015 pS5   Tyler Barnes

Various in vivo studies have investigated the insulin response that is
elicited when glutamate is elevated in circulation or in a given tissue;
fewer studies have investigated the effects of glutamate on glucose
uptake and handling.

Work from our lab suggests that glutamate
ingestion in humans can attenuate rises in blood glucose following a
carbohydrate load (75 g of Trutol®) compared with administration of
a carbohydrate load alone; this attenuated rise in glucose, following
a combined carbohydrate and glutamate load, occurred in absence of
increases in serum insulin concentrations.

However, the underlying mechanisms have yet to be investigated. To elucidate the effects of
glutamate on glucose handling in skeletal muscle tissue, differentiated
rat L6 myocytes were treated with increasing doses of glutamate
for 1 hr and glucose uptake was assessed by the addition of
[3H]-2-Deoxyglucose in HBS for 10 min. Cells treated with 2 mM, 1 mM,
and 500 M glutamate significantly increased [3H]-2-DG uptake by
129 ± 7%, 123 ± 5%, and 121 ± 4%, respectively relative to the control
condition (P<0.05). To evaluate the effect of treatment time on glucose
uptake, cells were incubated with 2 mM of glutamate for various
times ranging from 0 to 120 minutes. Treating cells for 30 minutes
resulted in the greatest increase in [3H]-2-DG uptake versus the control
condition (143 ± 9%, P<0.001), while cells treated for 45 and 60 minutes
also significantly increased [3H]-2-DG uptake (125 ± 9% and 129 ± 7%,
respectively; P<0.05). To investigate select mechanisms by which glutamate
acts to increase glucose uptake, cells were treated with 2 mM of
glutamate for 30 minutes with either a PI3K inhibitor (LY294002), PKC
inhibitor (BMD I), or AMPK inhibitor (Compound C). Compound C
reduced glucose uptake in cells treated with glutamate to a similar
extent as the control condition (98 ± 2%), whereas cells treated with
LY294002 showed significantly greater uptake than the control (128 ±
5%, P<0.05).

Our findings suggest that when muscle cells are exposed
to increased glutamate concentrations, glucose uptake into these cells
is augmented through AMPK activation.
This study will provide a basis
for future animal and human studies exploring the interactions of
glutamate and glucose in skeletal muscle.

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