Citations: 1-2
<1>
Authors
Ballard TC. Farag A. Branum GD. Akwari OE. Opara EC.
Institution
Department of Surgery, Duke University Medical Center, Durham, North Carolina
27710, USA.
Title
Effect of L-glutamine supplementation on
impaired glucose regulation during intravenous lipid administration [see
comments].
Comments
Comment in: Nutrition 1996 May;12(5):375
Source
Nutrition. 12(5):349-54, 1996 May.
Abstract
In contrast to L-glutamine, lipid emulsions are routinely
administered to patients receiving nutritional support. The provision of fat
during intravenous feeding is essential, but the potentially toxic byproducts
of fatty acid oxidation may have adverse metabolic consequences. In the
present study, we have examined the effect of L-glutamine,
an inhibitor of fatty acid oxidation, on the development of defective blood
glucose regulation caused by a 48-hour infusion of 10% intralipid in rats.
Male Sprague-Dawley rats (200-290 g) were anesthetized with sodium
pentobarbital, the right femoral vein cannulated, and baseline blood samples
were taken. Each rat was placed in a metabolic cage with access to water, in
the presence or absence of rodent chow. Two hours after waking, the rats were
infused with 10% intralipid with either saline (control), 2%
L-glutamine, or 2% L-alanine. After 48 hours, all animals
were sacrificed and blood samples were again obtained. The mean +/- SEM
plasma glucose levels before and after lipid infusion at the rate of 1 mL/hr
in control rats fed ad libitum, were 125 +/- 13 and 170 +/- 5 mg/dL (p <
0.01, n = 7). Similarly, plasma free fatty acids (FFA) in these animals rose
from 0.74 +/- 0.11 to 1.34 +/- 0.32 mmol/L (p < 0.05). Plasma insulin levels
also increased from 337 +/- 44 to 1278 +/- 88 pg/mL (p < 0.01). Reduction of
intralipid dose infusion did not prevent insulin resistance characterized by
hyperglycemia and hyperinsulinemia. However, addition of
L-glutamine to the high-dose lipid infusion with chow
feeding prevented changes in plasma glucose, insulin levels, and FFA but not
triglyceride levels. Also, glutamine but not alanine
supplementation in intralipid infused rats without chow
feeding prevented changes in plasma glucose, insulin, and malondialdehyde
levels. In conclusion, these data show that glutamine
supplementation during intravenous lipid administration in
rats prevents the development of impaired glucose regulation associated with
hyperlipidemia.
<2>
Authors
Opara EC. Petro A. Tevrizian A. Feinglos MN. Surwit RS.
Institution
Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.
Title
L-glutamine supplementation of a high fat
diet reduces body weight and attenuates hyperglycemia and hyperinsulinemia in
C57BL/6J mice.
Source
Journal of Nutrition. 126(1):273-9, 1996 Jan.
Abstract
C57BL/6J (B/6J) mice are genetically predisposed to become overweight and
develop hyperglycemia if raised on a high fat diet. The purpose of the
present study was to explore the effect of dietary
supplementation of L-glutamine (Gln), an
inhibitor of fatty acid oxidation, on the development of hyperglycemia and
excessive weight gain. Groups of 10 age- and weight-matched male B/6J mice
were raised on one of four diets: 1) a low fat, low sucrose (LL), studied
separately, 2) a high fat, low sucrose (HL) diet alone, 3) high fat, low
sucrose supplemented with L-glutamine (HL+Gln) and 4) high
fat, low sucrose supplemented with L-alanine (HL+Ala). Energy intake, body
weight, plasma glucose and insulin concentrations were monitored over time.
We found no difference in energy intake per unit body weight between any
groups after the first 2 wk of feeding. However, the mean +/- SEM for body
weight (27.1 +/- 0.6 g) of the LL group measured at 16 wk was lower (P <
0.05) than that of the HL group at 37.9 +/- 1.9 g. Also, after 5.5 mo, the
mean +/- SEM for plasma glucose and insulin concentrations in the LL group of
mice were 6.9 +/- 0.4 mmol/l and 146 +/- 30 pmol/l, which were lower (P <
0.05) than those in the HL group at 10.1 +/- 0.9 mmol/l and 438 +/- 84
pmol/l, respectively. Although both amino acids caused a 10% reduction (P <
0.05) in body weight compared with HL feeding at wk 16, only Gln
supplementation resulted in persistent reductions in both
plasma glucose and insulin concentrations over 5.5 mo. In another experiment,
when Gln was added to the high fat (HL) diet of heavy hyperglycemic animals
for 2 mo, body weight gain, hyperglycemia and hyperinsulinemia were
attenuated. In conclusion, supplementing glutamine to a high fat diet reduces
body weight and attenuated hyperglycemia and hyperinsulinemia in B/6J mice.