The Role of the Pancreas in the Induction of the Acute Catabolic State

Author(s):  
B. Vonen
Keyword(s):  
2001 ◽  
Vol 21 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Gonzalo Zevallos ◽  
Dimitrios G. Oreopoulos ◽  
Mitchell L. Halperin

Background Hyponatremia has a number of different causes; some may have serious untoward implications for patients undergoing chronic ambulatory peritoneal dialysis (CAPD). Objective To determine the pathophysiology of hyponatremia in patients on CAPD. Methods A retrospective analysis was carried out on 210 patients on CAPD. We selected patients with 2 – 4 consecutive periods when the plasma sodium concentration was ≤130 mmol/L and again when it was > 133 mmol/L. Exclusion criteria included hyperglycemia, orthostatic hypotension, edema, and inadequate records. Results An electrolyte-free water gain appeared to be the main cause of hyponatremia in only 1 of 5 patients because this was the only patient with a significant increase in body weight. In 1 patient, there was weight loss in the hyponatremic period, suggesting tissue catabolism was present. In 3 patients, there was neither weight gain nor evidence for a contracted extracellular fluid volume in the hyponatremic period, suggesting that intracellular potassium and phosphate loss could be the major mechanism for their hyponatremia. Conclusion When hyponatremia is due to a catabolic state, its management should aim to restore intracellular fluid composition ( i.e., to correct malnutrition).


2013 ◽  
Vol 45 (23) ◽  
pp. 1168-1185 ◽  
Author(s):  
J. David Furlow ◽  
Monica L. Watson ◽  
David S. Waddell ◽  
Eric S. Neff ◽  
Leslie M. Baehr ◽  
...  

Muscle atrophy can result from inactivity or unloading on one hand or the induction of a catabolic state on the other. Muscle-specific ring finger 1 (MuRF1), a member of the tripartite motif family of E3 ubiquitin ligases, is an essential mediator of multiple conditions inducing muscle atrophy. While most studies have focused on the role of MuRF1 in protein degradation, the protein may have other roles in regulating skeletal muscle mass and metabolism. We therefore systematically evaluated the effect of MuRF1 on gene expression during denervation and dexamethasone-induced atrophy. We find that the lack of MuRF1 leads to few differences in control animals, but there were several significant differences in specific sets of genes upon denervation- and dexamethasone-induced atrophy. For example, during denervation, MuRF1 knockout mice showed delayed repression of metabolic and structural genes and blunted induction of genes associated with the neuromuscular junction. In the latter case, this pattern correlates with blunted HDAC4 and myogenin upregulation. Lack of MuRF1 caused fewer changes in the dexamethasone-induced atrophy program, but certain genes involved in fat metabolism and intracellular signaling were affected. Our results demonstrate a new role for MuRF1 in influencing gene expression in two important models of muscle atrophy.


2013 ◽  
Vol 11 (1) ◽  
pp. 70-79 ◽  
Author(s):  
Georgios Tzanis ◽  
Stavros Dimopoulos ◽  
Varvara Agapitou ◽  
Serafim Nanas

2013 ◽  
Vol 4 (5) ◽  
pp. 495-500 ◽  
Author(s):  
Kasra Ahmadinia ◽  
Dongyao Yan ◽  
Michael Ellman ◽  
Hee-Jeong Im

AbstractBovine lactoferricin (LfcinB) is a multifunctional peptide derived from bovine lactoferrin that demonstrates antibacterial, antifungal, antiviral, antitumor, and immunomodulatory activities. Recently, studies have focused on the anti-catabolic and anti-inflammatory potential of LfcinB. LfcinB is able to modulate the effects cytokines such as IL-1 and fibroblast growth factor 2 as well as promote specific cartilage anabolic factors. These properties are particularly important in maintaining cartilage homeostasis and preventing a catabolic state, which leads to clinical pathology. This review focuses on the recent literature elucidating the role of LfcinB in preventing cartilage degradation.


2021 ◽  
Vol 22 (13) ◽  
pp. 7020
Author(s):  
Desirè Pantalone ◽  
Carlo Bergamini ◽  
Jacopo Martellucci ◽  
Giovanni Alemanno ◽  
Alessandro Bruscino ◽  
...  

Severe or major burns induce a pathophysiological, immune, and inflammatory response that can persist for a long time and affect morbidity and mortality. Severe burns are followed by a “hypermetabolic response”, an inflammatory process that can be extensive and become uncontrolled, leading to a generalized catabolic state and delayed healing. Catabolism causes the upregulation of inflammatory cells and innate immune markers in various organs, which may lead to multiorgan failure and death. Burns activate immune cells and cytokine production regulated by damage-associated molecular patterns (DAMPs). Trauma has similar injury-related immune responses, whereby DAMPs are massively released in musculoskeletal injuries and elicit widespread systemic inflammation. Hemorrhagic shock is the main cause of death in trauma. It is hypovolemic, and the consequence of volume loss and the speed of blood loss manifest immediately after injury. In burns, the shock becomes evident within the first 24 h and is hypovolemic-distributive due to the severely compromised regulation of tissue perfusion and oxygen delivery caused by capillary leakage, whereby fluids shift from the intravascular to the interstitial space. In this review, we compare the pathophysiological responses to burns and trauma including their associated clinical patterns.


Animals ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 137
Author(s):  
Ewa Tomaszewska ◽  
Natalia Burmańczuk ◽  
Piotr Dobrowolski ◽  
Małgorzata Świątkiewicz ◽  
Janine Donaldson ◽  
...  

The effect of alpha-ketoglutaric acid (AKG) supplementation to experimentally-induced, perinatal growth-retarded piglets was examined. Sows were treated with a synthetic glucocorticoid (Gc) during the last 25 days of pregnancy, and after the birth, piglets were randomly divided into three groups depending on the treatment. The Gc/Gc + AKG and Gc/AKG groups born by Gc-treated sows after the birth were treated with Gc or Gc + AKG for 35 days. Significantly lower serum growth hormone, IGF-I, osteocalcin, leptin, and cortisol concentrations were observed in the Gc/Gc + AKG group, while the bone alkaline phosphatase activity was significantly higher. Serum insulin concentration was higher in the control group. Serum alanine, lysine, histidine, and tryptophan concentrations were higher in the Gc/Gc + AKG and Gc/AKG groups. The perinatal action of Gc significantly affects histomorphometry of articular cartilage and trabecular bone and bone mechanics. The results clearly showed that dietary AKG had positive effects with regards to the profile of free amino acids. Taking into account the function of AKG as an energy donor and stimulator of collagen synthesis, it can be concluded that the anabolic role of AKG may be the main mechanism responsible for its protective effect against the GC-induced perinatal intensified catabolic state.


JAMA ◽  
1966 ◽  
Vol 195 (12) ◽  
pp. 1005-1009 ◽  
Author(s):  
D. J. Fernbach
Keyword(s):  

JAMA ◽  
1966 ◽  
Vol 195 (3) ◽  
pp. 167-172 ◽  
Author(s):  
T. E. Van Metre

2018 ◽  
Vol 41 ◽  
Author(s):  
Winnifred R. Louis ◽  
Craig McGarty ◽  
Emma F. Thomas ◽  
Catherine E. Amiot ◽  
Fathali M. Moghaddam

AbstractWhitehouse adapts insights from evolutionary anthropology to interpret extreme self-sacrifice through the concept of identity fusion. The model neglects the role of normative systems in shaping behaviors, especially in relation to violent extremism. In peaceful groups, increasing fusion will actually decrease extremism. Groups collectively appraise threats and opportunities, actively debate action options, and rarely choose violence toward self or others.


Sign in / Sign up

Export Citation Format

Share Document