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Congestive Heart Failure
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
The most common symptoms with RV failure include fatigue and ankle swelling. There may be a “fullness” of the neck or abdomen. Liver congestion can cause right upper quadrant abdominal discomfort. Stomach or intestinal congestion causes anorexia, early satiety, and bloating of the abdomen. If there is severe biventricular failure, skeletal muscle wasting may occur. This can reflect increased catabolism because of higher cytokine production. If a patient has extreme cardiac cachexia, the likelihood of death is increased. For older patients, atypical manifestations include confusion, delirium, falling, nighttime urinary incontinence, sudden declines in function, and sleep disturbances. HF can worsen any concurrent cognitive impairment or depression. Tachycardia and tachypnea may occur with LV failure. Severe LV failure may cause the patient to be visibly cyanotic or dyspneic, hypotensive, and agitated or confused due to hypoxia and insufficient cerebral perfusion. Some of these symptoms occur more often in older patients. Severe hypoxemia is reflected by central cyanosis that affects all of the body. Low blood flow with increased oxygen extraction is signified by peripheral cyanosis of the lips, fingers, and toes.
Functions of the Liver
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The breakdown of glucose to carbon dioxide and water with the production of energy is called glycolysis. Glucose catabolism proceeds by two pathways, either by cleavage to trioses producing pyruvic acid and lactic acid (the Embden–Meyerhof pathway) or via oxidation and decarboxylation to pentose (hexose monophosphate shunt). The net energy gain from glycolysis is three molecules of ATP. Pyruvic acid enters the citric acid cycle by conversion to acetic acid with the loss of one molecule of CO2. The citric acid cycle generates 12 molecules of ATP for every molecule of acetic acid. In total, 38 molecules of ATP are produced by the aerobic breakdown of glucose to pyruvate and its incorporation into the citric acid cycle. Pyruvic acid can be formed from the metabolism of amino acids and fat. Glycolysis produces acetyl CoA, which is used as a substrate for lipogenesis and subsequently the production of triglycerides. Another important property of the liver is the formation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) via the pentose phosphate pathway. Two NADPH molecules and ribose-5-phosphate are produced from one glucose molecule. NADPH is required for microsomal and mitochondrial hydroxylation of steroid hormones and biotransformation of many drugs.
Disease Prediction and Drug Development
Published in Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam, Introduction to Computational Health Informatics, 2019
Arvind Kumar Bansal, Javed Iqbal Khan, S. Kaisar Alam
There are two types of pathways: metabolic and cell signaling. Metabolic pathways have two major classes of reactions: 1) catabolic – breaking down complex molecules into simpler molecules; 2) anabolic – synthesizing complex molecules from simpler molecules. In addition, reactions store and release energy in a biochemical form. Cellular respiration is an example of catabolic reaction. In cellular respiration, sugar is imported in the cells, and energy is released after the reaction.
Cyanidin attenuates the apoptosis of rat nucleus pulposus cells and the degeneration of intervertebral disc via the JAK2/STAT3 signal pathway in vitro and in vivo
Published in Pharmaceutical Biology, 2022
Xiaoliang Bai, Meichao Jiang, Jie Wang, Shuai Yang, Zhiwei Liu, Hongxin Zhang, Xiaojuan Zhu
Aggrecan and collagen II are the main components of the nucleus pulposus ECM that play important roles in maintaining the elasticity and osmotic pressure of the disc (Xu et al. 2019). IVDD is often accompanied by degradation of the ECM, which is caused by the imbalance in the synthesis and catabolism of the ECM (Tao et al. 2016). Catabolism is mainly controlled by proteolytic enzymes, of which MMPs and ADAMTSs play the key role (Wang et al. 2015). Besides, the decrease in the number of NPCs caused by excessive apoptosis plays a pivotal role in the pathogenesis of IVDD (Zhao et al. 2017). Factors such as mechanical load, nutritional deficiencies, hyperglycaemia, and pro-inflammatory factors (TNF-α, IL-1β) can induce apoptosis in NPCs. In contrast, anti-IVDD factors, such as resveratrol, platelet-derived growth factor (PDGF), transforming growth factor-β1 (TGF-β1), reduce IVDD by inhibiting NPCs apoptosis (Li et al. 2008). Inhibiting the apoptosis of NPCs and promoting the synthesis of ECM components to inhibit the initiating factors of IVDD are expected to become the key to treat IVDD (Cai et al. 2016; Chen et al. 2018).
Correlation between serum trimethylamine-N-oxide concentration and protein energy wasting in patients on maintenance hemodialysis
Published in Renal Failure, 2022
Chun Hu, Yumei Zhang, Xiao Bi, Lu Yao, Yueling Zhou, Wei Ding
PEW is highly prevalent in ESRD patients, with a prevalence of 30–75% among patients on hemodialysis [20]. Several signaling pathways and humoral factors have been discovered to be involved in CKD-induced PEW, including the ubiquitin proteasome system (UPS), myostatin/activin pathway, endogenous glucocorticoids, insulin-like growth factor 1 (IGF-1) pathway, metabolic acidosis, and persistent inflammation [21–23]. In our previous study, we also showed that mitochondrial dysfunction/NLRP3 inflammasome axis may contribute to angiotensin II-induced skeletal muscle wasting, the use of siRNA or genetic depletion of NLRP3, mitochondria-targeted antioxidant, or PPAR-γ agonists significantly normalized muscle function and the protein energy balance [24,25]. The factors associated with these pathways lead to decreased anabolism and/or increased catabolism, which increases resting energy expenditure and causes hypermetabolism, eventually leading to progressive muscle wasting. Uremic toxins, which are organic solutes normally metabolized and excreted by the kidneys, often accumulated in the presence of impaired kidney function, causing body toxicity [26]. However, to date, there are few published reports on gut microbiota-dependent metabolite TMAO in patients with CKD, and the association between TMAO concentrations and PEW/muscle wasting has not been investigated.
The triglyceride-glucose index as a novel marker associated with sarcopenia in non-diabetic patients on maintenance hemodialysis
Published in Renal Failure, 2022
Ruoxin Chen, Liuping Zhang, Mengyan Zhang, Ying Wang, Dan Liu, Zuolin Li, Xiaoliang Zhang, Hui Jin, Bicheng Liu, Hong Liu
Kidneys are recipient organs of signaling molecules from skeletal muscle mass [19]. There are two main mechanisms for muscle mass loss in CKD: (1) increased muscle catabolism via the activation of, among others, the ubiquitin-proteasome system, caspase-3, and lysosomes pathways; (2) impaired muscle growth, regeneration, repair, and suppression of protein synthesis with components of abnormal myogenesis [20]. The development of sarcopenia in patients undergoing MHD is mainly due to the alteration of multiple factors that regulate the balance between catabolism and anabolism in muscle, probably due to the uremic environment caused by ESKD [21]. The factors of sarcopenia in ESKD are complex, including insulin resistance, inflammation, malnutrition, abnormal myogenic regulatory factors, increased myostatin, and decreased physical activity [22–24]. Under the influence of multiple factors, the persistent imbalance between muscle anabolism and catabolism can lead to protein degradation and muscle atrophy, which in turn affects muscle structure and function [25,26]. Notably, the mechanisms of sarcopenia in dialysis patients are complex and remain a research direction worthy of future consideration.