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New Developments in Oral Insulin Delivery
Published in Emmanuel Opara, Controlled Drug Delivery Systems, 2020
Alec Jost, Mmesoma Anike, Emmanuel Opara
Once released from beta cells, insulin potentiates changes in cellular activity via the insulin receptor, an intrinsic tyrosine kinase receptor. Binding and dimerization allow for the phosphorylation of multiple intracellular signaling molecules. In general, the changes associated with insulin receptor activation induce a cellular state favoring energy storage via protein, triglyceride, and glycogen synthesis. However, the specifics of insulin’s action vary depending on target tissue. In muscle, insulin induces glycogen synthesis and suppresses protein catabolism, as well as upregulating cell surface glucose transporter-4 (GLUT4) receptors allowing for an increased uptake of extracellular glucose. Muscle plays a primary role in glucose clearance and storage; it is thought to be responsible for 60%–70% of insulin-mediated glucose uptake. In adipose tissue, insulin stimulates lipogenesis and GLUT4 translocation to the membrane, accounting for ~10% of glucose uptake mediated by insulin. In hepatic tissue, glycogen synthesis increases while gluconeogenesis and ketone body production are inhibited by insulin. The liver is responsible for up to 30% of postprandial glucose clearance, highlighting the importance of hepatic insulin delivery in the generation of appropriate glucose handling mechanisms and physiologic energy storage. Insulin also plays roles in the brain, kidneys, and vascular endothelium, and while these roles pertain less directly to serum glucose handling, they still may represent active contributors to the pathogenesis of diabetes (De Meyts 2000).
Microbial Biotechnology
Published in Nwadiuto (Diuto) Esiobu, James Chukwuma Ogbonna, Charles Oluwaseun Adetunji, Olawole O. Obembe, Ifeoma Maureen Ezeonu, Abdulrazak B. Ibrahim, Benjamin Ewa Ubi, Microbiomes and Emerging Applications, 2022
Olawole O. Obembe, Nwadiuto (Diuto) Esiobu, O. S. Aworunse, Nneka R. Agbakoba
The microbiomes of lean and obese people vary in the sense that obese people possess lower microbial diversity as against the richer diversity of lean people. Metagenomic analysis on 16S rRNA of the human gut microbiome has shown that the microbiome of obese persons has an abundance of phylum Firmicutes and a reduced abundance of the Bacteroidetes. So, an alteration in the gut environment that warrants changes in the Bacteroidetes/Firmicutes ratio provides genetic material that enables individuals to have the capacity to harvest energy from the diet. This disturbance consequently promotes lipogenesis, leading to an increase in the quantity of the lipid droplets and eventually to excess weight gain.
Potential of Oleaginous Microorganisms in Green Diesel Production
Published in V. Sivasubramanian, Bioprocess Engineering for a Green Environment, 2018
R. Selvaraj, I. Ganesh Moorthy, V. Sivasubramanian, R. Vinoth Kumar, R. Shyam Kumar
The steps in lipid accumulation in yeast are (1) the production of acetyl CoA and (2) the conversion of acetyl CoA into lipids. Acetyl CoA is generated in the mitochondria and transferred to the cytosol. Lipogenesis is the process by which fatty acids are synthesized from acetyl-CoA in the cytosol.
Evaluation of sucrose-enriched diet consumption in the development of risk factors associated to type 2 diabetes, atherosclerosis and non-alcoholic fatty liver disease in a murine model
Published in International Journal of Environmental Health Research, 2021
Carolina Gabriela Plazas Guerrero, Selene De Jesús Acosta Cota, Francisco Humberto Castro Sánchez, Marcela De Jesús Vergara Jiménez, Efrén Rafael Ríos Burgueño, Juan Ignacio Sarmiento Sánchez, Lorenzo Antonio Picos Corrales, Ulises Osuna Martínez
To know the factors involve in the development of NASH is fundamental in the understanding of this condition and for creating effective therapies to prevent and cope with this disease (Arguello et al. 2015; Walenbergh and Shiri-Sverdlov 2015). However, the mechanisms contributing to this transition are not completely known. In this context, the ‘multiple-hit’ model has been proposed to explain this phenomenon (Buzzetti et al. 2016; Fang et al. 2018). According to this model, insulin resistance causes an increase in hepatic de novo lipogenesis and in lipolysis in adipose tissue with increased flux of fatty acids to the liver and altered secretion of adipokines and inflammatory cytokines (Buzzetti et al. 2016). TG accumulate excessively and lipotoxicity increases derived from high levels of fatty acids, cholesterol among other lipid metabolites leading to mitochondrial dysfunction and oxidative stress (Fang et al. 2018). Overall with the increased absorption of fatty acids and other pathogenic molecules from a dysfunctional gut to the liver leads to a chronic hepatic inflammatory state (Kirpich et al. 2015) which could progress to cell death and fibrosis (Caballero et al. 2009; Walenbergh and Shiri-Sverdlov 2015; Vega-Badillo 2016).
Mechanisms of beneficial effects of exercise training on non-alcoholic fatty liver disease (NAFLD): Roles of oxidative stress and inflammation
Published in European Journal of Sport Science, 2019
Parvin Farzanegi, Amir Dana, Zeynab Ebrahimpoor, Mahdieh Asadi, Mohammad Ali Azarbayjani
Numerous studies showed that exercise training significantly decreases intrahepatic fat contents. The underlying mechanism involves β-oxidation and lipogenesis (Figure 1). Recent investigations have indicated that exercise activity can regulate hepatic lipid metabolism by regulating hepatic β-oxidation and lipogenesis (Jeppesen & Kiens, 2012). Rector et al. (2008) indicated that exercise training increases hepatic fatty acid oxidation in NAFLD rats by increasing acetyl-coenzyme A carboxylase (ACC) phosphorylation and cytochrome c contents, indicating a possible enhancement of the final steps of oxidative phosphorylation. They also showed that exercise training decreases hepatic lipogenesis by reducing fatty acid synthase (FAS) and ACC contents (Rector et al., 2008). ACC is the committed step in fatty acid synthesis, catalysing the carboxylation of acetyl-CoA to form malonyl-CoA. ACC phosphorylation inhibits its activity and reduces formation of malonyl-CoA. Reduced content of malonyl-CoA is associated with increase in fatty acid oxidation and decrease in available substrate for FAS. Koves et al. (2005) found that exercise training increased the flux of both β-oxidation and tricarboxylic acid (TCA) cycle in the skeletal muscle. These data suggest that exercise training can enhance the complete oxidation of lipids in both the liver and the skeletal muscle.
Biochanin A prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced adipocyte dysfunction in cultured 3T3-L1 cells
Published in Journal of Environmental Science and Health, Part A, 2019
Eun Mi Choi, Kwang Sik Suh, So Young Park, Sang Ouk Chin, Sang Youl Rhee, Suk Chon
As PPARγ plays an important role in adipocyte differentiation, it is recognized as the master regulator of adipogenesis. Activation of PPARγ triggers the expression of various genes that are closely related to lipogenesis, fatty acid synthesis, and energy metabolism.[19] Adiponectin, an adipocyte-derived hormone that is expressed in differentiated adipocytes, stimulates lipid accumulation and insulin-responsive transporters.[20] Adiponectin plays an important role in the regulation of glucose and lipid metabolism. In differentiated adipocytes, adiponectin over-expressing cells exhibit greater fat accumulation, and stimulate glucose uptake by activating GLUT4. Because adiponectin is induced by PPAR-γ activity, adiponectin is used as a marker of PPAR-γ efficacy.[21] Thus, an increase in adiponectin secretion has more favorable effects against insulin resistance.[22] Here, we found that biochanin A partially reverses the TCDD-induced decrease in PPARγ and adiponectin levels during differentiation of 3T3-L1 adipocytes, suggesting that biochanin A affects adipogenesis and lipid accumulation by modulating PPAR-γ signaling and adiponectin production.