Download or read book Studies on the Changes in Hepatic Lipid Metabolism Induced by Fat Feeding written by William Washington Webster and published by . This book was released on 1959 with total page 158 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Fat Detection written by Jean-Pierre Montmayeur and published by CRC Press. This book was released on 2009-09-14 with total page 646 pages. Available in PDF, EPUB and Kindle. Book excerpt: Presents the State-of-the-Art in Fat Taste TransductionA bite of cheese, a few potato chips, a delectable piece of bacon - a small taste of high-fat foods often draws you back for more. But why are fatty foods so appealing? Why do we crave them? Fat Detection: Taste, Texture, and Post Ingestive Effects covers the many factors responsible for the se

Download or read book Diet and Health written by National Research Council and published by National Academies Press. This book was released on 1989-01-01 with total page 765 pages. Available in PDF, EPUB and Kindle. Book excerpt: Diet and Health examines the many complex issues concerning diet and its role in increasing or decreasing the risk of chronic disease. It proposes dietary recommendations for reducing the risk of the major diseases and causes of death today: atherosclerotic cardiovascular diseases (including heart attack and stroke), cancer, high blood pressure, obesity, osteoporosis, diabetes mellitus, liver disease, and dental caries.

Download or read book A Comprehensive Overview of the Effects of Diet on the Hepatic Transcriptome and Translatome in Rat Liver written by Jaclyn Welles and published by . This book was released on 2021 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Consumption of excess calories is associated with alterations in lipid and carbohydrate metabolism in the liver, and often leads to development of metabolic diseases in the liver such as, non-alcoholic steatohepatitis (NASH), non-alcoholic fatty liver disease (NAFLD), and diabetes. Even though hepatic lipid accumulation begins with as little as 1-wk of high-fat diet i.e. HFD consumption, previous studies searching for the mechanism(s) involved have focused almost universally on time points >=1 month. Moreover, no studies have assessed possible changes in mRNA translation as a mechanism involved in hepatic fatty acid accumulation, even though changes in mRNA translation have been shown to explain ~40% of alterations in protein expression. Thus, for the studies presented in this thesis, we hypothesized that the translation of specific mRNAs essential in the regulation of metabolic processes in the liver, may be detrimentally dysregulated, contributing to the onset and pathogenesis of metabolic diseases. In chapter 3 we hypothesized that short-term (i.e. 2-wk) consumption of a Western-diet (WD), high in saturated fat, sucrose, and cholesterol, significantly alters the translation of specific mRNA transcripts e.g. lipoprotein lipase (LPL), hormone sensitive lipase E (LIPE), and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), in the liver, contributing to the onset of metabolic disorders such as NASH and NAFLD. Notably, the 5' and 3' untranslated region (UTR) of all 3 mRNAs contain regulatory motifs e.g., upstream open reading frames (uORF), internal ribosomal entry sites (IRES), terminal oligopyrimidine (TOP) motif, which may be modulating their translational control as observed in studies performed in chapter 3. Moreover, the expression of several mRNAs i.e. LPL, LIPE, glucokinase (GCK), and fibroblast growth factor 21 (FGF21), was significantly lower in the livers of both fasted and refed rats fed a WD, when compared to rats fed a CD. Overall, the results presented in chapter 3 suggest that alterations in liver metabolism occur rapidly after placing rats on a WD, and that such changes manifest as a consequence of alterations in gene expression occurring at both the transcriptional and translational levels. Surprisingly, feeding-induced phosphorylation of 4E-BP1 and S6, was blunted in WD-fed rats when compared to CD, suggesting that hepatic mTORC1 activity may be, at least in part, responsible for some of the translational changes observed in this study. Thus, the changes observed between fasted and refed CD and WD-fed rats, suggest that the results demonstrating modulations in the expression, and/or translation of several mRNAs, critical in function in the regulation of metabolic processes (i.e. glucose and lipid metabolism), may be occurring through a mechanism dependent oft hepatic mTORC1-activity. Interestingly, in studies performed in chapter 3, the expression of FGF21 mRNA was significantly upregulated in the livers of fasted rats when compared to refed rats, a finding previously demonstrated in studies found in the literature. Studies recently published by Cyphert et. al. demonstrated how the fasting secretagogue glucagon increased the secretion of FGF21 into the media in three hepatoma cell lines, without affecting total FGF21 mRNA abundance suggesting either translational or post-translational control of FGF21 mRNA translation in the liver. Notably, several studies have found that in cases of obesity, glucagon concentrations are significantly dysregulated, leading to glucagon-dependent changes, such as changes in liver weight, hepatic triglycerides, gluconeogenesis, and glycogenolysis. Moreover, in studies where mice lacking the expression of the glucagon receptor (GCGR), were challenged using diet-induced obesity (DIO) by HFD, or streptozotocin treatments to model Type 2 Diabetes, mice lacking GCGR expression, were protected against hyperglycemia, beta cell loss, and hepatic steatosis, directly associating glucagon activity with improvements in metabolic control (93). Together, these findings delineate glucagon as a potential therapeutic against diet-induced obesogenic pathologies. Thus, we hypothesized that FGF21 mRNA was being translationally upregulated by glucagon in the liver. Notably, results from studies performed in chapter 4 of this thesis, demonstrated how the translation and secretion of FGF21 was significantly upregulated by the peptide hormone, glucagon, in rat H4IIE hepatoma cells. Furthermore, glucagon also inhibited mTORC1 activity concurrently with upregulation of FGF21 mRNA secretion, suggesting a mechanism which may be dependent on mTORC1 activity in the liver. Finally, we also observed significant increases in the translation of FGF21 mRNA in the livers of fasted rats when compared to refed, changes independent of changes to total FGF21 mRNA abundance. All in all, results from these studies highlight mRNA translation, as a method of gene regulation, which may be influencing the onset and pathogenesis of metabolic diseases driven by the liver. Studies are currently underway exploring possible regulatory motifs in RNA e.g. uORFs; 5'-TOP; IRES; RNA binding, motifs that may be coordinating translational control of mRNAs identified in chapters 3 and 4.

Download or read book Adipose Tissue Lipolysis and the Regulation of Hepatic Lipid Metabolism written by Sicheng Zhang and published by . This book was released on 2023 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: The communication between adipocytes and liver plays a crucial role in the physiological regulation of metabolism and understanding the basis of this dynamic inter-organ communication has the potential to advance clinical therapies. This is particularly important for conditions like obesity, fatty liver disease, and type 2 diabetes, which have emerged as global metabolic disorders. Consequently, the investigation of the communication between the liver and adipose tissue has been a hot point in metabolic research for many years (Azzu, Vacca et al. 2020).Numerous studies have investigated adipose tissue and its secretome composition, however, a comprehensive global analysis of the lipidome was still absent. In this study, we used the beta-3-adrenergic receptor agonist, CL-316,243 (CL), to stimulate adipose tissue lipolysis in both in vivo and in vitro settings (Zhang, Williams et al. 2023). A single dose of CL treatment was deemed an appropriate model to mimic acute adipose tissue lipolysis. Additionally, we conducted a time course analysis to investigate the dynamic changes in the adipose tissue lipolysis lipidome and its impact on hepatic lipidome, considering the lipid flux originating from adipose tissue lipolysis. We also utilized ATGL adipose tissue-specific knockout mice as a model to underscore the significance of adipose tissue lipolysis in hepatic lipid remodeling (Kim, Tang et al. 2016). Our study provides a comprehensive perspective on how adipose tissue lipolysis remodels the hepatic lipidome. Furthermore, we identified specific lipid alterations of interest, including the accumulation of linoleic acid and the release of odd-chain free fatty acids. Another pivotal aspect of the study on the interaction between adipose tissue and the liver is how the liver responds to adipose tissue lipolysis. In this investigation, we applied RNA-seq and subsequent bioinformatic analysis to detect novel hepatic regulators. In addition to the well-established regulators such as PPARa, HNF4a, and SREBP1c, we identified hepatic glucocorticoid receptor (GR) as another critical transcription factor involved in this process, which is activated by the hypothalamic-pituitary adrenal (HPA) axis. Furthermore, it appears that hepatic GR plays a crucial role in regulating ketogenesis and triglyceride accumulation during adipose tissue lipolysis. Notably, our research revealed that Plin5 serves as a downstream target whose expression is controlled by hepatic GR directly. And absence of hepatic Plin5 also impedes ketogenesis. This suggests that the Adipose-HPA-GR-PLIN5 axis may represent an important regulatory pathway in ketogenesis. In addition to RNA-seq, we employed Assay of Transposase-Accessible Chromatin ATAC-seq as an additional tool to investigate hepatic regulators. Our findings suggest that a novel transcription factor, Elk4, may potentially have a role in hepatic metabolism, specifically in glucose metabolism and pyruvate metabolism. However, given the limited knowledge available about Elk4, further research is warranted to understand more about its functions and mechanisms.

Download or read book Management of Dyslipidemia written by Wilbert S. Aronow and published by BoD – Books on Demand. This book was released on 2021-07-21 with total page 176 pages. Available in PDF, EPUB and Kindle. Book excerpt: Dyslipidemia is a major risk factor for cardiovascular events, cardiovascular mortality, and all-cause mortality. The earlier in life dyslipidemia is treated, the better the prognosis. The current book is an excellent one on dyslipidemia written by experts on this topic. This book includes 12 chapters including 5 on lipids, 4 on hypercholesterolemia in children, and 3 on the treatment of dyslipidemia. This book should be read by all health care professionals taking care of patients, including pediatricians since atherosclerotic cardiovascular disease begins in childhood.

Download or read book Studies in Lipid Metabolism written by Sister John Magdalen Young and published by . This book was released on 1968 with total page 384 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book The Effects of Ethanol and Several Naturally Occurring Metabolites on Hepatic Lipid Metabolism in Rats written by Steven Scott Hannah and published by . This book was released on 1993 with total page 206 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Using a Rat Nutritional Model of Non alcoholic Fatty Liver Disease to Study the Effects of Variations in Iron on Hepatic Lipid Metabolism and Vice Versa written by Umbreen Ahmed and published by . This book was released on 2009 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: [Truncated abstract] Iron and lipid metabolism are connected albeit the relationship involved is poorly understood. Variations in iron stores lead to inappropriate lipogenesis and processing of lipoproteins by hepatocytes. Conversely, dietary fat affects iron status. Hepatic damage has been demonstrated when iron and lipid deposition increases. It has been proposed that iron overload by generating oxidative stress causes lipid peroxidation and this is involved in the generation/progression of non-alcoholic fatty liver disease/non-alcoholic steatohepatitis (NAFLD/NASH). On the other hand NASH is also associated with increased hepatic iron loading and altered iron metabolism. It was the original intention of this research to study the derangement of iron metabolism in the background of NAFLD/NASH using the rat Lieber model, and to see whether there is progression of NAFLD/NASH with iron loading. The Lieber model was expected to develop NASH, however the rats developed a less progressed condition and remained within a range of NAFLD type I-II. Chapter 3 reports that although there was steatosis there was no inflammatory cell infiltrate and no increase in mRNA expression of proinflammatory cytokines, markers of oxidative stress and endoplasmic reticulum (ER) stress. These differences probably represent variation in the genetic background of the rats and/or other environmental factors. Failure to develop NASH in these rats necessitated a change in direction of the thesis and the data were then assessed from the perspective of the effects that lipids have on hepatic iron metabolic pathways and vice versa. Experiments were conducted to assess different dietary fat loads in combination with variations in iron treatment on lipid and iron metabolism, ranging from iron deficiency to iron loading. Chapter 5 shows that consuming a standard diet (35% fat) increased plasma lipids according to the level of iron present. Hepatic triglycerides (TG) were decreased with iron deficiency. Iron dextran injections loaded predominantly macrophages and produced occasional foci of lipid droplets with no inflammatory cell infiltrates. The mRNA expression of oxidative stress responsive genes, proinflammatory cytokines, ER stress genes, lipogenic regulatory/effector genes were not affected and there was no sign of apoptosis, indicating that iron loading from normal in combination with a 35% fat containing diet did not develop NAFLD. In Chapter 6 the same iron loading used in Chapter 5 was given with the high fat diet (71% fat) shown in Chapter 3 to produce NAFLD type II. Within this range of fatty liver, iron loading mainly of macrophages did not exacerbate the extent of NAFLD. Iron deficiency in combination with a high fat diet reduced hepatic lipid deposition, increased lipogenic gene expression and increased serum TG, suggesting that iron deficiency increased secretion and decreased peripheral clearance of lipoproteins. Chapter 7 compared the standard and high fat diets with variations in iron loading to gain insight into the mechanisms involved in the development of NAFLD type II. ER stress genes were increased in high fat groups suggesting it to be an important player for the generation of NAFLD...

Download or read book Do Dietary Fats Contribute to Fatty Liver written by Connor Andrew Mahler and published by . This book was released on 2021 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Non-alcoholic fatty liver disease (NAFLD) is a common occurrence in people with insulin resistance and NAFLD increases the risk of developing liver disease. Although the pathogenesis of NAFLD is not well understood, recent evidence suggests that mitochondria dysfunction is critical in its development. A dominant species of cardiolipin in the inner mitochondria membrane is tetra-linoleoyl-cardiolipin (LA4CL), a phospholipid with molecules of linoleic acid (LA). Reduced levels of LA4CL are linked with mitochondrial dysfunction. The hepatic phospholipid fatty acid profiles may reflect both the disease of NAFLD as well as dietary fat composition. The overall hypothesis of my thesis is: consumption of a linoleic acid (LA) rich oil will alleviate progression of fatty liver in mice by increased incorporation of LA into hepatic phospholipids. To test this hypothesis, we fed mice two different high fat diets, one containing a LA rich safflower oil and the other diet containing lard. To determine any changes in hepatic fat accumulation we measured triglyceride (TG), and total lipid content. Phospholipid fatty acid composition was assessed as well to determine any changes in phospholipid fatty acids. C57BL6/J male mice (N=24) were assigned to a high fat diet of 24% wt fat containing either LA-rich safflower oil or lard which is rich in saturated fat, for 130 days. Body composition, blood glucose and insulin sensitivity measurements were assessed. Solid phase extraction (SPE) and gas chromatography were used to analyze the fatty acid composition of the hepatic phospholipids; HPLC/MS in collaboration with Dr. Genevieve Sparagna (University of Colorado) was used to determine cardiolipin speciation. An insulin tolerance test revealed that blood glucose remained lower at 90 min and 120 min after the insulin injection in the SO diet compared to the LD diet. The SO diet had increased the percent of LA4CL compared to the LD diet of total cardiolipin species. No differences in total lipids or TG in the liver between diets. Of the phospholipid fractions extracted, the fatty acid compositions reflected major species of fatty acids found in their respective diets in the phospholipid fractions reported. This study indicates that dietary fat altered fatty acid compositions of phospholipids, and consumption of a high fat LA-rich safflower oil does not alleviate fatty liver accumulation in mice fed a high fat diet.

Download or read book Changes in Fatty Acids Profiles After Three Weeks of High fat Diet Feeding in Obesity prone Rats written by Tzu-Wen Liu and published by . This book was released on 2013 with total page 110 pages. Available in PDF, EPUB and Kindle. Book excerpt: High-fat diet (HFD) feeding is commonly used in animal models to induce obesity and metabolic diseases. However, the effect of HFD on serum fatty acid profiles remains unclear. Changes in serum fatty acid profiles due to HFD may be a factor in lipotoxicity in various organs. Historically, in vitro studies have utilized individual non-esterified fatty acids (NEFA) to study lipid exposure, potentially ignoring the importance of fatty acid combinations on cellular lipid metabolism. OBJECTIVE: To accurately characterize the proportion of circulating fatty acids entering and exiting the liver in obese-prone rats fed with HFD in both fasted and fed state. Our ultimate goal is to create a physiological relevant fatty acid mixture to investigate lipid exposure in a cell culture system. METHODS: Obesity prone rats were fed a HFD (60%kcal fat) or a control diet (10%kcal fat) for 3 weeks; liver, portal and systemic blood samples were collected. Triglycerides (TG) and NEFA in the serum, TG, diglycerides (DG) and phospholipids (PL) in the liver were extracted and analyzed using gas chromatography. RESULTS: HFD group was heavier and had bigger fat pad compared to control diet fed animals. Both systemic and portal serum TG were ~40% lower in HFD. In contrast, liver had higher fasting TG (~2-fold) and DG (~1.3-fold) in the HFD group compared to control group. Total serum NEFA levels were not affected by diet in the fasted state, but increased in the HFD group compared to the control group under fed state. In the control group, monounsaturated fatty acids (MUFA) were the predominant fatty acids in serum TG, whereas polyunsaturated fatty acids (PUFA) were the dominant fatty acids in the HFD group. The elevations of PUFA were mostly attributed to the increased of n-6 PUFA, linoleic acid and arachidonic acid. Similar shift from MUFA to n-6 PUFA also occurred in the serum NEFA fraction. CONCLUSION: HFD shifted predominate fatty acids of serum TG fraction from MUFA in the control diet to n-6 PUFA. A more physiologically relevant fatty acid mixture to mimic HFD conditions for in vitro studies may include increased linoleic acid and arachidonic acid relative to saturated fatty acids and MUFA.

Download or read book Exogenous Lipids Regulate the Development of Hepatic Steatosis in a Lean NAFLD Model fed a High Carbohydrate Diet written by Kuan-Hsun Huang and published by . This book was released on 2016 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Non-alcoholic fatty liver disease (NAFLD), an umbrella term that encompasses hepatic steatosis, steatohepatitis, fibrosis, and cirrhosis, has become the most common chronic liver disease in the developed countries. NAFLD has been shown to be positively associated with obesity, and thus not surprisingly the majority of NAFLD studies have utilized obese models to explore NAFLD causality. However, previous studies indicated that 25% of patients with NAFLD are not obese and that 7.4% of lean adults have steatosis, and they are more likely to be younger and female, suggesting that these people with lean NAFLD were metabolically obese. Additionally, insulin resistance is an independent risk factor to the development of lean NAFLD, which has been shown to be related to cardiovascular disease and diabetes mellitus. Therefore, understanding the etiology of lean NAFLD in the early stage of the development of steatosis becomes an urgent need. On the other hand, lifestyle modification intervention including diet and physical activity is believed to improve NAFLD or even reverse it, but very few studies have focused on the reversal of hepatic steatosis in the lean NAFLD model. Thus, the overall research hypothesis in this dissertation is that the exogenous lipids as a form of lipid emulsion (LE) and physical activity are capable to reverse hepatic triacylglycerol (TG) accumulation in the lean mouse model with preexisting steatosis.Previous work in our laboratory indicated that 13.5% (percent of total energy, en-%) Intralipid given orally ameliorated TG accumulation in the liver of nonobese mice fed a high carbohydrate diet (HCD) for 5 weeks. Here, in my first study (chapter 3) I examined whether HCD can induce hepatic steatosis in a short period of time (8d) and whether Intralipid and voluntary exercise can prevent liver triacylglycerol (TG) accumulation by regulating the de novo lipogenesis-associated transcripts and the concentrations of total fatty acids, in 8 d, on the development of steatosis in a lean mouse model. The results revealed that hepatic TG contents in the HCD-fed mice were significantly increased, confirmed by Oil Red O staining, suggesting the 8d period of induction of steatosis was sufficient to induce mild steatosis. Supplementation with 13.5% Intralipid, with or without exercise, also suppressed HCD-induced steatosis. qRT-PCR analysis showed that including 13.5% Intralipid to the HCD significantly decreased the transcript levels for lipogenesis-associated genes, whereas mice-fed HCD with exercise had less beneficial effect in the early stage of steatosis, as compared to HCD supplemented with 13.5% Intralipid. Fatty acid profiling also showed a consistency with transcriptional data that the concentration of monounsaturated FA was decreased significantly. As noted in the previous study that HCD is capable to induce mild hepatic steatosis within 8d, I conducted a second study (chapter 4) to test whether the beneficial effect contributed by 13.5% Intralipid supplementation will be extended to the mouse with preexisting steatosis. To investigate this, the mice were fed a HCD for 2.5 weeks to establish hepatic steatosis, then switched to HCD+13.5%LE for the final 2.5 wk. A combined targeted biochemical and untargeted metabolomics approach was employed, and biochemical analyses revealed that hepatic TG level and the lipogenic genes were significantly decreased in mice fed HCD with 13.5% Intralipid. Total fatty acids and metabolomic profiles in liver and plasma indicated that the mice fed a HCD supplemented with 13.5% Intralipid exhibited reduced hepatic lipogenesis, but increases in hepatic Krebs cycle intermediates, and in plasma very-low density lipoprotein. Many studies have shown that n-3 and n-9 FA have beneficial effects on lipid metabolism. In a third study (chapter 5), I compared 3 LEs-- Intralipid, Omegaven and ClinOleic-- for their ability to reverse hepatic TG accumulation after the onset of steatosis. At this time, we used biochemical, transcriptomic and metabolomic approaches to capture an overall metabolic change in the lean NAFLD mouse model. The results showed that HCD-induced hepatic steatosis did not develop insulin resistance and that 13.5% Omegaven had the strongest reversal effect on hepatic TG accumulation, as well as on the genes involved in the hepatic glucose and lipid metabolism, which can further maintain energy homeostasis in the mice with preexisting steatosis. Additionally, lipolysis in the adipose tissue was greatly improved by introduction of Omegaven; the metabolites, assayed by nuclear magnetic resonance spectroscopy, were consistent with the transcriptomic data, suggesting a plausible mechanism of how n-3 FA-based LE reversed hepatic steatosis. In summary, adding 13.5% Intralipid to a HCD not only prevents the development of steatosis in the early dynamic stage by reducing de novo lipogenesis, but also mitigates the preexisting hepatic steatosis and energy homeostasis in the liver in a 5-wk study. However, Omegaven provides beneficial effect on the reversal of preexisting steatosis as well as an improvement on energy homeostasis in both liver and adipose tissue.

Download or read book Lipid Metabolism in the Liver Adipose and Muscle with Glucocorticoids and how These Organs Can Regulate Each Other written by Wangkuk Son and published by . This book was released on 2021 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Background: The Western diet is characterized by a high amount of n-6 PUFA and low n-3 PUFA. Due to the structural difference of composing fatty acid, Omega-3 PUFAs have beneficial effects while omega-6 PUFAs elicit adverse effects on lipid metabolism, building the foundation of metabolic syndrome and various diseases. Objective: Determine whether fat composition in an HFD affects GC-induced alterations in lipid handling by the liver, adipose tissue, and skeletal muscle. Methods: Male wild-type C57BL/6 mice were randomized into two groups: n-6 (45% fat 177.5 g lard) and n-3 (45% fat 177.5 g Menhaden oil). After 4 weeks on their diets, groups were divided to receive either daily injections of dexamethasone (3 mg/kg/day) or sterile PBS for 1 week while continuing diets. Results: Omega-3 HFD diet ameliorates adipocyte hypertrophy and hepatic fatty accumulation by involving associated lipid metabolism markers (CD36 and FABP). Conclusion: The present study's result demonstrated that the change of fat composition in HFD could beneficially alter the fatty acid accumulation, adipocyte size, and associated lipid metabolism markers..

Download or read book Prevention of CLA induced Insulin Resistance and Nonalcoholic Fatty Liver Disease by Docosahexaenoic Acid in Mice written by Dawn Fedor and published by . This book was released on 2013 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Insulin resistance (IR) is a condition in which normal amounts of insulin fail to maintain normal blood glucose because of decreased responsiveness of muscle (glucose uptake), liver (inhibition of gluconeogenesis) and adipocytes (inhibition of lipolysis). IR is often associated with nonalcoholic fatty liver disease (NAFLD), the most common liver disease in adults and children in the Western world. Results from human epidemiological studies indicate that n-3 PUFA reduce the development of IR and NAFLD although the mechanisms involved are poorly understood. Our lab previously showed that concomitant supplementation of 1.5% docosahexaenoic acid (22:6 n-3; DHA) with 0.5% t10, c12- conjugated linoleic acid (18:2 n-6; CLA) prevented the CLA-induced NAFLD and IR. The effective dose of DHA, the mechanisms involved and the effect of CLA on fatty acid compositions of adipose tissue and muscle, and whether DHA can prevent those CLA-induced changes in fatty acid composition is not known. In the first study, we examined the ability of DHA (0.5 and 1.5%) to prevent increases in NAFLD and homeostatic model assessment of insulin resistance (HOMA-IR) induced by CLA (0.5%) when fed concomitantly for 4 weeks to C57BL/6N female mice. We also examined changes in expression of hepatic genes involved in fatty acid synthesis and oxidation. CLA supplementation increased liver triglycerides (TG) and HOMA-IR by 221 and 547%, respectively, and decreased mass of adipose depots by 65-90%. When fed concomitantly, 0.5% and 1.5% DHA prevented CLA-induced increases in liver TG and circulating insulin with varying efficiency, but neither dose of DHA prevented the loss in adipose tissue mass. In CLA + DHA 0.5 % group the liver TG did not differ from those in the control group, but circulating insulin and HOMA-IR were 285 and 264 %, respectively, greater than those in the control group. In the CLA + DHA 1.5% group liver TG were 54% lower than those in the control group, but circulating insulin concentration and HOMA-IR did not differ between these two groups. CLA increased the expression of hepatic genes involved in fatty acid synthesis and decreased the expression of genes involved in fatty acid oxidation. 1.5% DHA prevented changes in the expression of hepatic genes caused by CLA, which may be a possible mechanism contributing to the prevention of TG accumulating in the liver. Based on these results, we further studied the 1.5% DHA diet. We investigated the effects of 1.5% DHA concomitantly fed with CLA on fatty acid compositions of liver, adipose, and muscle lipids in the same mice, as well as expression of genes involved in adipose fatty acid metabolism. CLA supplementation decreased total hepatic n-3 PUFA concentration. DHA not only prevented the CLA-induced changes in liver fat, but also increased n-3 PUFA by >350% as compared with the control group. CLA decreased adipose weight and the expression of genes involved in fatty acid synthesis, oxidation, and uptake, and increased that of UCP2 in the adipose. Supplementing DHA along with CLA increased adipose n-3 PUFA by >1000% compared with control group, but did not prevent the CLA-induced changes in mass or gene expression. Both CLA and DHA were incorporated into muscle lipids, but had minor effects on FA composition. In conclusion, liver, adipose tissue, and muscle responded differently to CLA and DHA supplementation. CLA was more potent than DHA in altering depot fat and insulin concentration. DHA prevented CLA-induced increase in liver fat but not loss of adipose mass. CLA and DHA were preferentially incorporated into adipose tissue lipids, but they had only modest effects on the overall fatty acid composition of the adipose tissue. The largest changes in fatty acid composition were seen in the liver and smallest in muscle lipids.

Download or read book Obesity and Lipotoxicity written by Ayse Basak Engin and published by Springer. This book was released on 2017-06-05 with total page 618 pages. Available in PDF, EPUB and Kindle. Book excerpt: Due to the resultant health consequences and considerable increase in prevalence, obesity has become a major worldwide health problem. “Obesity and Lipotoxicity” is a comprehensive review of the recent researches to provide a better understanding of the lipotoxicity-related mechanisms of obesity and the potential for the development of new treatment strategies. This book overviews the biochemical pathways leading to obesity-related metabolic disorders that occur subsequent to lipotoxicity. Chapters examine the deleterious effects of nutrient excess at molecular level including the cellular and molecular aspects of breast cancer, resistance to leptin, insulin, adiponectin, and interconnection between the circadian clock and metabolic pathways during high-fat feeding. “Lipotoxicity and Obesity” will be a useful resource for clinicians and basic science researchers, such as biochemists, toxicologists, immunologists, nutritionists, adult and pediatric endocrinologists, cardiologists, as well as students who are thought in this field.

Download or read book Lipids and Cardiovascular Disease written by and published by . This book was released on 1990 with total page 226 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Fish Oil Replacement and Alternative Lipid Sources in Aquaculture Feeds written by Giovanni M. Turchini and published by CRC Press. This book was released on 2010-07-19 with total page 542 pages. Available in PDF, EPUB and Kindle. Book excerpt: Experts are predicting that demand for marine fish oil will soon outstrip supply, creating extreme urgency within the global aquafeed industry to find viable alternatives. Fish Oil Replacement and Alternative Lipid Sources in Aquaculture Feeds is the first comprehensive review of this multifaceted, complex issue. It also addresses the crucial quest