Glutamine nitrogen kinetics in insulin-dependent diabetic humans

1991 ◽  
Vol 261 (6) ◽  
pp. E713-E718 ◽  
Author(s):  
D. Darmaun ◽  
M. Rongier ◽  
J. Koziet ◽  
J. J. Robert

To assess the effect of insulin deficiency on whole body glutamine kinetics, five young adults with type I (insulin-dependent) diabetes received 4-h primed continuous infusions of L-[1-13C]leucine and L-[2-15N]glutamine in the postabsorptive state after blood glucose had been clamped overnight at either a normoglycemic level (approximately 85 mg/dl) or a moderate hyperglycemic level (approximately 260 mg/dl) by means of an automated glucose control insulin infusion system. The hyperglycemic state was associated with a significant rise in leucine level [from 165 +/- 23 to 242 +/- 62 (SD) microM], appearance rate (from 125 +/- 11 to 142 +/- 17 mumol.kg-1.h-1), and oxidation (from 27 +/- 10 to 31 +/- 10 mumol.kg-1.h-1). In contrast, neither the plasma level nor the appearance rate of glutamine (333 +/- 51 vs. 318 +/- 58 mumol.kg-1.h-1) was affected. We conclude that insulin deficiency resulting in moderate hyperglycemia induces a 13% rise in whole body proteolysis and yet does not stimulate glutamine de novo synthesis, despite increased precursor availability.

Diabetes ◽  
1985 ◽  
Vol 34 (1) ◽  
pp. 67-73 ◽  
Author(s):  
J. J. Robert ◽  
B. Beaufrere ◽  
J. Koziet ◽  
J. F. Desjeux ◽  
D. M. Bier ◽  
...  

1983 ◽  
Vol 102 (4) ◽  
pp. 557-560
Author(s):  
W. L. Clarke ◽  
T. W. Melton ◽  
G. M. Bright

Abstract. The effect of sustained hyperglucagonaemia on blood glucose concentrations and on insulin requirements was evaluated in 6 fasting insulin dependent diabetic subjects whose blood glucose concentrations were being controlled with a closed loop insulin infusion system. Subjects were iv infused initially with either saline or glucagon and subsequently with the other infusate. All determinations were performed following the period during which transient increases in glucagon stimulated glucose production have been reported to occur. Plasma glucagon concentrations were significantly higher during the glucagon study period (491±65 vs 70±13 pg/ml ± sd, P<0.001) as were blood glucose concentrations(104 ± 2 vs 84 ± 7 mg/ml ± sd, P<0.001) and insulin requirements (3.5 to 36.5 vs 0 to 2.3 mU/kg/h, P<0.05). Sustained hyperglucagonaemia continues to have an effect on glucose homeostasis for at least 2 h following the initiation of a continuous infusion.


Diabetes ◽  
1985 ◽  
Vol 34 (1) ◽  
pp. 67-73 ◽  
Author(s):  
J. J. Robert ◽  
B. Beaufrere ◽  
J. Koziet ◽  
J. F. Desjeux ◽  
D. M. Bier ◽  
...  

Diabetes ◽  
1985 ◽  
Vol 34 (11) ◽  
pp. 1127-1133 ◽  
Author(s):  
R. K. Mayfield ◽  
P. V. Halushka ◽  
H. J. Wohltmann ◽  
M. Lopes-Virella ◽  
J. K. Chambers ◽  
...  

1999 ◽  
Vol 277 (4) ◽  
pp. E597-E607 ◽  
Author(s):  
Cornelia C. Metges ◽  
Antoine E. El-Khoury ◽  
Lidewij Henneman ◽  
Klaus J. Petzke ◽  
Ian Grant ◽  
...  

We have investigated whether there is a net contribution of lysine synthesized de novo by the gastrointestinal microflora to lysine homeostasis in six adults. On two separate occasions an adequate diet was given for a total of 11 days, and a 24-h (12-h fast, 12-h fed) tracer protocol was performed on the last day, in which lysine turnover, oxidation, and splanchnic uptake were measured on the basis of intravenous and oral administration ofl-[1-13C]lysine andl-[6,6-2H2]lysine, respectively. [15N2]urea or15NH4Cl was ingested daily over the last 6 days to label microbial protein. In addition, seven ileostomates were studied with15NH4Cl. [15N]lysine enrichment in fecal and ileal microbial protein, as precursor for microbial lysine absorption, and in plasma free lysine was measured by gas chromatography-combustion-isotope ratio mass spectrometry. Differences in plasma [13C]- and [2H2]lysine enrichments during the 12-h fed period were observed between the two15N tracer studies, although the reason is unclear, and possibly unrelated to the tracer form per se. In the normal adults, after15NH4Cl and [15N2]urea intake, respectively, lysine derived from fecal microbial protein accounted for 5 and 9% of the appearance rate of plasma lysine. With ileal microbial lysine enrichment, the contribution of microbial lysine to plasma lysine appearance was 44%. This amounts to a gross microbial lysine contribution to whole body plasma lysine turnover of between 11 and 130 mg ⋅ kg−1 ⋅ day−1, depending on the [15N]lysine precursor used. However, insofar as microbial amino acid synthesis is accompanied by microbial breakdown of endogenous amino acids or their oxidation by intestinal tissues, this may not reflect a net increase in lysine absorption. Thus we cannot reliably estimate the quantitative contribution of microbial lysine to host lysine homeostasis with the present paradigm. However, the results confirm the significant presence of lysine of microbial origin in the plasma free lysine pool.


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