China
Africa
Explore chapters and articles related to this topic
Mitigation of Obesity: A Phytotherapeutic Approach
Published in Amit Baran Sharangi, K. V. Peter, Medicinal Plants, 2023
A.B. Sharangi, Suddhasuchi Das
Altered lipid metabolic processes together with lipogenesis and lipolysis facilitate the development of obesity (Pagliassotti et al., 1997). Synthetic moieties and surgical procedures are the universal therapy of obesity, but have detrimental side effects and likelihood of severe recurrence (Karri et al., 2019). Lipogenesis stores free fatty acids in the form of triglyceride (Mandrup and Lane, 1997); whereas in lipolysis, the stored triglyceride is metabolized to free fatty acids and glycerol (Ducharme and Bichel, 2008). Obesity is accompanied by an abnormally high concentration of lipids in blood, i.e., hyperlipidemia (Akiyama et al., 1996). The adipose tissue secretes several biologically active adipokines and thereby regulates metabolism and homeostasis (Yudkin et al., 1999). Three key transcription factors like peroxisome proliferator-activated receptor (PPAR), CCAAT/enhancer-binding protein (C/EBP) and sterol regulatory element-binding protein (SREBP) regulate the expression of these lipid-metabolizing enzymes during adipose tissue development (Freytag and Utter, 1983). 5’ AMP-activated protein kinase (AMPK) plays a major role in lipid and glucose metabolism by inactivating acetyl-CoA carboxylase (ACC) and Through up-regulating the expression of carnitine palmitoyl transferase-1 (CPT-1), PPAR, and uncoupling protein, stimulation of fatty acid oxidation is done (Kim et al., 2007).
Insulin Signaling Modulates Neuronal Metabolism
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Qian Huang, Jialin Fu, Kelly Anne Borges, Weikang Cai
One of the major anabolic effects of insulin in the body is to potently promote de novo lipogenesis (100–102). Such anabolic effect of insulin is particularly important in the brain, due to the restrictive entry of the circulating cholesterol and long-chain fatty acids through BBB. Thus, almost all the cholesterol in the brain is synthesized in situ and is essential for normal brain development and function. Decreased cholesterol biosynthesis in the brain caused by chemical or genetic intervention has been shown to impair normal brain development, synaptic transmission, and memory in mice (103–105). Mechanistically, insulin promotes neuronal cholesterol and long-chain fatty acid biosynthesis through direct and indirect pathways (Figure 3.2). Thus, insulin directly enhances the transcription of genes involved in cholesterol and long-chain fatty acyl-CoA biosynthesis in neurons (105, 106). Alternatively, insulin stimulates the transcription of the same class of genes in astrocytes to upregulate cholesterol and long-chain fatty acid production (103, 105–107), which can be transferred to neurons in the form of ApoE-containing lipoproteins (108, 109). Therefore, when glucose supply is abundant postprandially, insulin signals both neurons and astrocytes to reroute carbon source from glucose to the biosynthesis of cholesterol and long-chain fatty acids. Such anabolic action of insulin would facilitate the replenishment of damaged neuronal plasma membranes and remodeling of synapses, thus beneficial for healthy and normal neural functions.
Nonalcoholic Fatty Liver Disease
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
Fat accumulation in the liver also can be stimulated by fructose consumption inducing oxidative stress in the mitochondria. Acontinase-2 and enoyl CoA hydrase are enzymes found in the mitochondria that are sensitive to oxidative stress (Jensen et al. 2018). Fructose and uric acid decrease acontinase-2 activity, leading to the accumulation of citrate, which moves into the cytoplasm, stimulates ATP citrate lyase, and activates lipogenesis (Jensen et al. 2018). This can also impair fatty acid oxidation by decreasing enoyl CoA hydratase-1 activity, which stimulates AMP Deaminase-2 and reduces AMP-activated protein kinase, which regulates enoyl CoA hydratase-1. This results in accumulation of fat and stimulation of gluconeogenesis (Jensen et al. 2018).
Comparative study of dietary fat: lard and sugar as a better obesity and metabolic syndrome mice model
Published in Archives of Physiology and Biochemistry, 2023
Victor Hugo Dantas Guimarães, Deborah de Farias Lelis, Luis Paulo Oliveira, Luciana Mendes Araújo Borém, Felipe Alberto Dantas Guimarães, Lucyana Conceição Farias, Alfredo Mauricio Batista de Paula, André Luiz Sena Guimarães, Sérgio Henrique Sousa Santos
In our study, the high-fat/high-sugar diet treatment was correlated with increased total adiposity and body weight. As Ferreira et al. demonstrated, these diets modulate the lipogenic and lipolysis pathways. The authors found that mice fed a high-carbohydrate diet displayed increased lipogenic activity, while high-fat fed mice displayed decreased lipolytic activity (Ferreira et al.2014). These findings might indicate that the combined diets, as used in our study, may exacerbate body composition alterations by concomitantly altering these antagonist pathways towards energy storage. The high-fat/high-sugar diet treatment also induced glucose intolerance, decreased insulin sensitivity, and concomitantly increased glucose fasting levels. These findings explain the increased body weight and total adiposity observed in the treated animals, as glucose is one of the main lipogenesis and inflammation inducers (Jameel et al.2014), thus reinforcing the appearance of metabolic syndrome-associated characteristics, such as dyslipidemia and hyperglycaemia, in our obesity mice models. Yang and colleagues (2012) also reported that a high-fat/high-sugar diet is able to induce metabolic syndrome associated complications, mainly by altering lipogenesis, insulin signalling, and inflammatory pathways in mice (Yang et al.2012).
Methylglyoxal impairs β-adrenergic signalling in primary rat adipocytes
Published in Archives of Physiology and Biochemistry, 2022
Tomasz Szkudelski, Aleksandra Cieślewicz, Katarzyna Szkudelska
The accumulation of lipids in cells of adipose tissue involves two processes, i.e. lipogenesis and lipolysis. Evidence from rodent studies indicates that MG can negatively affect adipose tissue (Dhar et al.2011, Rodrigues et al.2013, 2017, Matafome et al.2017), however, its short-term influence on adipocyte metabolism was not previously studied. Lipogenesis is largely stimulated by insulin. Results of in vitro studies demonstrate that MG may disturb the regulatory action of this hormone. Prolonged exposure of 3T3-L1 adipocytes to MG was shown to diminish insulin-induced glucose uptake, and also to impair the insulin signalling pathway (Jia et al.2006, Jia and Wu 2007, Vidal et al.2012). Moreover, MG may change the structure of insulin, which is also associated with deterioration of its action (Jia et al.2006). In order to determine short-term effects of MG on the action of this hormone in primary rat adipocytes, insulin-induced glucose conversion to lipids was studied. The first step of this process is intracellular glucose transport (via glucose transporter GLUT4), followed by its metabolism and formation of triglycerides. It was shown that insulin-induced lipogenesis from glucose was unaffected by MG. The lack of influence on lipogenesis allows us to suppose that glucose transport is also unaltered. These results indicate that 2-h exposure of adipocytes to MG is insufficient to disturb the lipogenic effects of insulin.
Effects of short-term fasting and pharmacological activation of AMPK on metabolism of rat adipocytes
Published in Archives of Physiology and Biochemistry, 2021
Tomasz Szkudelski, Katarzyna Szkudelska
The cells of white adipose tissue, adipocytes, store large amounts of energy in the form of lipids. Adipocytes release glycerol and fatty acids or, depending on the actual demand of the organism, synthesise triglycerides from glycerol, fatty acids, and glucose. This is an important feature and thereby adipose tissue is an important element of whole-body energy homeostasis (Luo and Liu 2016). It is well established that dysregulation of the balance between lipogenesis and lipolysis is associated with insufficient or exaggerated accumulation of fat tissue in the body (Frühbeck et al. 2014). The latter effect leads to overweight or obesity and a risk of insulin resistance. Moreover, the link between excessive adipose tissue accumulation and inflammation is recently well established (Jung and Choi 2014). Adipose tissue secretes also adipokines, which have a relevant regulatory role. Thereby, adipose tissue is involved in the regulation, among others, of feeding behaviour and energy expenditure (Luo and Liu 2016). The rate of lipogenesis and lipolysis in the adipocytes, and also secretion of adipokines changes depending on various conditions. Under physiological conditions, these processes are strongly affected by hormones, circadian activity and the resulting changes in food ingestion, physical activity, and fasting. Energy deprivation is known to affect adipocyte lipid storage and also secretion of adipokines. Fasting is associated with reduced lipogenesis and increased lipolysis, and also with changes in secretion of some adipokines (Luo and Liu 2016).