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      Fat-free mass change after nutritional rehabilitation in weight losing COPD: role of insulin, C-reactive protein and tissue hypoxia

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          Fat-free mass (FFM) depletion marks the imbalance between tissue protein synthesis and breakdown in chronic obstructive pulmonary disease (COPD). To date, the role of essential amino acid supplementation (EAAs) in FFM repletion has not been fully acknowledged. A pilot study was undertaken in patients attending pulmonary rehabilitation.


          28 COPD patients with dynamic weight loss > 5% over the last 6 months were randomized to receive EAAs embedded in a 12-week rehabilitation program (EAAs group n = 14), or to the same program without supplementation (C group n = 14). Primary outcome measures were changes in body weight and FFM, using dual X-ray absorptiometry (DEXA).


          At the 12th week, a body weight increment occurred in 92% and 15% of patients in the EAAs and C group, respectively, with an average increase of 3.8 ± 2.6 kg ( P = 0.0002) and −0.1 ± 1.1 kg ( P = 0.81), respectively. A FFM increment occurred in 69% and 15% of EAAs and C patients, respectively, with an average increase of 1.5 ± 2.6 kg ( P = 0.05) and −0.1 ± 2.3 kg ( P = 0.94), respectively. In the EAAs group, FFM change was significantly related to fasting insulin (r 2 0.68, P < 0.0005), C-reactive protein (C-RP) (r 2 = 0.46, P < 0.01), and oxygen extraction tension (PaO 2x) (r 2 = 0.46, P < 0.01) at end of treatment. These three variables were highly correlated in both groups (r > 0.7, P < 0.005 in all tests).


          Changes in FFM promoted by EAAs are related to cellular energy and tissue oxygen availability in depleted COPD. Insulin, C-RP, and PaO 2x must be regarded as clinical markers of an amino acid-stimulated signaling to FFM accretion.

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          Most cited references 5

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          Daily body mass variability and stability in active men undergoing exercise-heat stress.

          The purpose of this study was to quantify the variability and stability of 1st morning body mass (BM) fluctuations during daily exercise in the heat while following traditional fluid intake guidance. Data from 65 men were examined retrospectively. BM fluctuations were monitored over 4 to 15 consecutive days. Group daily variation in BM was 0.51+/-0.20 kg. Group coefficient of variation was 0.66+/-0.24%, normally distributed, and not related to either absolute BM (r = 0.04) or number of measurements (r = 0.34). Three days resulted in a similar variability estimate compared to 6 or 9 d, although precision was improved with 9 d. In conclusion, 3 consecutive BM measurements provide an accurate assessment of daily BM variability, which is less than 1% for active men when replacing 100% of sweat losses during exercise. The data also suggest that daily BM is a sufficiently stable physiological parameter for potential daily fluid balance monitoring.
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            Short-term regulation of insulin-mediated glucose utilization in four-day fasted human volunteers: role of amino acid availability.

            Glucose homeostasis in men fasted for 84 h was assessed using isotopes, indirect calorimetry and forearm balance techniques during a basal period and three sequential hyperinsulinaemic euglycaemic clamps each lasting for 150 min. Two protocols (n = 12 in each) were used: subjects were either allowed to develop hypoaminoacidaemia or received a commercial solution of L-amino acids while maintaining near-basal plasma leucine levels. Insulin infusions resulted in 3-, 35- and 650-fold increases in plasma insulin levels in both protocols. The infusion of amino acids produced a rightward shift in the dose-response curve of insulin's effect on suppressing hepatic glucose production, indicating decreased sensitivity in addition to blunting of the maximal responsiveness. Total body glucose rate of disappearance was progressively increased with escalating insulin doses, but was 22% lower at the intermediate and highest insulin doses in the group that was infused with amino acids (3.44 +/- 0.53 vs 4.82 +/- 0.71 and 7.72 +/- 1.01 vs 10.36 +/- 1.08, respectively; p less than 0.05). Forearm balance data confirmed the isotopic data, since amino acid infusions blunted the insulin-mediated increase in net forearm glucose utilization (by 50-83%). Furthermore, the infusion of amino acids resulted in marked reductions in the rate of carbohydrate oxidation and storage as assessed by indirect calorimetry. The data indicate that the amino acid-mediated suppression of glucose utilization and carbohydrate oxidation is exerted on the responsive component of insulin action.
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              Effect of hyperinsulinemia on amino acid utilization and oxidation independent of glucose metabolism in the ovine fetus.

              We studied the effect of acute hyperinsulinemia on amino acid (AA) utilization and oxidation rates independent of insulin-enhanced glucose metabolism in fetal sheep. Metabolic studies were conducted in each fetus (n = 11) under three experimental periods. After control period (C) study, a fetal hyperinsulinemic-euglycemic-euaminoacidemic (HI-euG-euAA) clamp was established, followed by a hyperinsulinemic-hypoglycemic-euaminoacidemic (HI-hypoG-euAA) clamp to decrease glucose metabolic rates toward C values. Infusions of (3)H(2)0, L-[1-(13)C]leucine, and [(14)C(U)]glucose were administered to measure blood flow, leucine oxidation, and fetal glucose uptake, utilization, and oxidation in each period. Fetal glucose utilization rate increased 1.7-fold with hyperinsulinemia (C 5.8 +/- 0.8, HI-euG-euAA 10 +/- 1.3, P < 0.0001), returning to rates not different from C with hypoglycemia (HI-hypoG-euAA 7.1 +/- 0.9 vs. C value, P = 0.15). Fetal glucose oxidation rate increased 1.7-fold with hyperinsulinemia (C 3.1 +/- 0.2, HI-euG-euAA 5.4 +/- 0.4, P < 0.0001) and decreased to near control rates with hypoglycemia (4.0 +/- 0.3 HI-hypoG-euAA vs. C value, P = 0.006). AA utilization rates increased with hyperinsulinemia for all essential and most nonessential AAs (P < 0.001) and did not change when insulin-induced increases in glucose utilization returned to control rates. Leucine oxidation rate increased 1.7-fold with hyperinsulinemia (C 1.0 +/- 0.3 micromol.min(-1).kg(-1), HI-euG-euAA 1.7 +/- 0.3 micromol.min(-1).kg(-1), P < 0.002) and did not change when glucose oxidation rate was decreased with hypoglycemia. These results demonstrate that, in fetal sheep, insulin promotes AA utilization and oxidation independent of its simultaneous effects on glucose metabolism. In acute hyperinsulinemic conditions, AA oxidation does not change when insulin-induced glucose utilization is prevented.

                Author and article information

                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                18 February 2010
                : 5
                : 29-39
                Department of Pneumology and Biomedical Engineering, Scientific Institute of Montescano, Salvatore Maugeri Foundation I.R.C.C.S. Pavia, Italy
                Author notes
                Correspondence: Simonetta Baldi, U.O. di Riabilitazione Specialistica – Pneumologia Riabilitativa, Istituto Scientifico di Montescano, Fondazione S Maugeri, IRCCS, Via Per Montescano no. 31, 27040 Montescano (Pavia) Italy, Tel +39 0385 247227, Fax +39 0385 61386, Email simonetta.baldi@
                © 2010 Baldi et al, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

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