scholarly journals Insulin sensitivity of muscle protein metabolism is altered in patients with chronic kidney disease and metabolic acidosis

2015 ◽  
Vol 88 (6) ◽  
pp. 1419-1426 ◽  
Author(s):  
Giacomo Garibotto ◽  
Antonella Sofia ◽  
Rodolfo Russo ◽  
Ernesto Paoletti ◽  
Alice Bonanni ◽  
...  
2009 ◽  
Vol 76 (7) ◽  
pp. 751-759 ◽  
Author(s):  
Xiaonan H. Wang ◽  
Jie Du ◽  
Janet D. Klein ◽  
James L. Bailey ◽  
William E. Mitch

2007 ◽  
Vol 32 (3) ◽  
pp. 426-433 ◽  
Author(s):  
Eric D.B. Goulet ◽  
Christine Lord ◽  
Jean-Philippe Chaput ◽  
Mylène Aubertin-Leheudre ◽  
Martin Brochu ◽  
...  

Insulin plays a pivotal role in skeletal muscle protein metabolism and its action decreases with age. A loss of muscle mass, termed sarcopenia, also occurs with age. The age-associated decline in insulin sensitivity (IS) may negatively alter muscle protein metabolism and, therefore, be implicated in the aetiology of sarcopenia. However, no studies have yet compared the level of IS between older individuals with or without sarcopenia. Thus, in this study, we compared the IS of 20 class I sarcopenics (CIS), 8 class II sarcopeniscs (CIIS), and 16 non-sarcopenics (NS), among a group of otherwise healthy, non-obese, postmenopausal women. IS was estimated with the quantitative IS check index (QUICKI). Muscle mass index (MMI), which was used to determine sarcopenia, was calculated as follows: (appendicular  muscle  mass × 1.19) – 1.01/h2, where h = height. Fat-free mass (FFM), fat mass (FM), and trunk FM (TFM) were measured by dual-energy X-ray absorptiometry. Accelerometry and indirect calorimetry were used to estimate resting (REE), daily (DEE), and physical activity (PAEE) energy expenditure. A 3 d food record was used to determine total energy, protein (animal and vegetal), and carbohydrate intakes. As expected, MMI and FFM differed significantly among groups. However, no significant differences were found among groups for IS, FM, TFM, REE, DEE, PAEE, or total energy, protein (both animal and vegetable), and carbohydrate intakes. Using QUICKI, a surrogate measure of IS, the present results suggest that the action of insulin does not play an important role in the development and maintenance of sarcopenia in healthy, non-obese, postmenopausal women.


2016 ◽  
Vol 94 (suppl_5) ◽  
pp. 709-709
Author(s):  
F. A. S. Silva ◽  
S. C. Valadares Filho ◽  
L. N. Rennó ◽  
S. A. Santos ◽  
D. Zanetti ◽  
...  

2000 ◽  
Vol 37 (4) ◽  
pp. 219-224 ◽  
Author(s):  
L. Luzi ◽  
L. Piceni Sereni ◽  
M. Spessot ◽  
R. Dodesini ◽  
M.R. Pastore ◽  
...  

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Ilter Bozaci ◽  
Ali Nazmi Can Doğan ◽  
Merve Aktar ◽  
Alev Mahşer ◽  
Gizem Yıldırım ◽  
...  

AbstractObjectivesMetabolic acidosis is a common disorder seen in course of chronic kidney disease (CKD). In this study, we aimed to investigate the association of Base excess (BE), Anion gap (AG) and Delta Ratio with progression of CKD, renal replacement therapy (RRT) requirement and mortality in patients with stage 3–5 CKD.MethodsA total of 212 patients with stage 3–5 CKD were included in this study. Patients were divided into two groups according to the baseline BE level. Patients were also grouped according to the delta ratio such as non- AG, High AG and mixed type.ResultsMean BE level was significantly lower (−4.7 ± 4.0 vs. −3.3 ± 4.3; p=0.02) in patients with CKD progression. The patients in group 1 (n: 130) (Be<−2.5) revealed more CKD progression (%53 vs. %32; p=0.002), and RRT requirement (%35 vs. %15; p=0.001). Baseline BE <−2.5 (odds ratio, 0.38; 95% CI, 0.16 to 0.91; p<0.05) and baseline GFR (odds ratio, 0.94; 95% CI, 0.90 to 0.97; p<0.001) were independently related to RRT requirement. Delta BE was independently associated with mortality (odds ratio, 0.90; 95% CI, 0.85–0.96; p<0.01).ConclusionsLow BE levels were associated with CKD progression and RRT requirement. BE change is associated with mortality during the follow-up of those patients.


2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
María M. Adeva-Andany ◽  
Carlos Fernández-Fernández ◽  
David Mouriño-Bayolo ◽  
Elvira Castro-Quintela ◽  
Alberto Domínguez-Montero

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.


Sign in / Sign up

Export Citation Format

Share Document