Fatty acid metabolism in segments of rat intestine

1965 ◽  
Vol 208 (4) ◽  
pp. 607-614 ◽  
Author(s):  
Daniel Porte ◽  
Cecil Entenman
Keyword(s):  
Small Intestine ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Sodium Taurocholate ◽  
Tissue Uptake ◽  
Rat Intestine ◽  
A Minor

The in vitro metabolism of albumin-bound palmitic acid-1-C14 by segments of small intestine was studied. Tissue uptake, esterification, and oxidation of the fatty acid were measured separately and found to respond independently to altered incubation conditions. Uptake was reversible, and did not require glucose or oxygen. It was not inhibited by fluoride or arsenate. Esterification required both glucose and oxygen, but was unaffected by insulin. It was depressed by succinate and almost completely inhibited by fluoride and arsenate. Oxidation was a minor fate for fatty acid. It was independent of glucose but inhibited by succinate, fluoride, and arsenate. Sodium taurocholate stimulated uptake, but not esterification, as has been previously reported. The possible significance of the reversible tissue uptake reaction is discussed.

Abstract 330: Glycogen Synthase Kinase-3a Negatively Regulates Fatty Acid Metabolism During Lipid-induced Insulin Resistance

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Michinari Nakamura ◽  
Junichi Sadoshima
Keyword(s):  
Insulin Resistance ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Fatty Acid Metabolism ◽  
Lipid Accumulation ◽  
Acid Metabolism ◽  
Glycogen Synthase ◽  
Acid Oxidation ◽  
Peroxisome Proliferator

Obesity and insulin resistance lead to ectopic lipid accumulation and impaired cardiac metabolism, resulting in cardiovascular diseases. Peroxisome proliferator-activated receptor α (PPARα) is highly expressed in the heart and serves as a key regulator of fatty acid metabolism. However, the underlying mechanisms responsible for the development of cardiac dysfunction in these pathologies are still poorly understood. GSK-3α was activated, as evidenced by a decrease in S21 phosphorylation, during insulin resistance with normoglycemia in the hearts of obese mice fed a high-fat diet and ob/ob mice. To evaluate the functional significance of GSK-3α upregulation with regard to metabolism, we applied 50 μM of BSA-conjugated palmitic acid to cardiomyocytes in vitro for three days. This intervention elicited ectopic lipid accumulation, as evaluated with Oil Red O staining, and a 2.0-fold activation of GSK-3α, similar to lipid-induced insulin resistance and dyslipidemia in the heart in vivo . In this condition, downregulation of GSK-3α with shRNA-GSK-3α in cardiomyocytes increased cell viability, ATP synthesis, and fatty acid oxidation, but not glycolysis. Downregulation of GSK-3α also increased the activity of PPRE-luciferase (1.5 fold, p<0.05) and mRNA expression of genes involved in fatty acid metabolism in response to palmitic acid, including Acox1 and Cpt1b . Overexpression of GSK-3α induced a rightward shift of the dose response curve where the activity of the PPARα reporter was plotted against the dose of WY14643, a PPARα agonist. GSK-3α, but not GSK-3β, directly interacted with and phosphorylated PPARα in vitro . Collectively, these results suggest that GSK-3α negatively regulates ligand-dependent activity of PPARα through phosphorylation of PPARα, thereby inhibiting fatty acid metabolism during lipid-induced insulin resistance. GSK-3α may be a novel therapeutic target for metabolic disorders.

scholarly journals Lipid and glucose metabolism in hepatocyte cell lines and primary mouse hepatocytes: a comprehensive resource for in vitro studies of hepatic metabolism

2019 ◽  
Vol 316 (4) ◽  
pp. E578-E589 ◽  
Author(s):  
Shilpa R. Nagarajan ◽  
Moumita Paul-Heng ◽  
James R. Krycer ◽  
Daniel J. Fazakerley ◽  
Alexandra F. Sharland ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Glucose Metabolism ◽  
Cell Lines ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Primary Hepatocytes ◽  
Primary Mouse Hepatocytes ◽  
Primary Mouse ◽  
Mouse Hepatocytes

The liver is a critical tissue for maintaining glucose, fatty acid, and cholesterol homeostasis. Primary hepatocytes represent the gold standard for studying the mechanisms controlling hepatic glucose, lipid, and cholesterol metabolism in vitro. However, access to primary hepatocytes can be limiting, and therefore, other immortalized hepatocyte models are commonly used. Here, we describe substrate metabolism of cultured AML12, IHH, and PH5CH8 cells, hepatocellular carcinoma-derived HepG2s, and primary mouse hepatocytes (PMH) to identify which of these cell lines most accurately phenocopy PMH basal and insulin-stimulated metabolism. Insulin-stimulated glucose metabolism in PH5CH8 cells, and to a lesser extent AML12 cells, responded most similarly to PMH. Notably, glucose incorporation in HepG2 cells were 14-fold greater than PMH. The differences in glucose metabolic activity were not explained by differential protein expression of key regulators of these pathways, for example glycogen synthase and glycogen content. In contrast, fatty acid metabolism in IHH cells was the closest to PMHs, yet insulin-responsive fatty acid metabolism in AML12 and HepG2 cells was most similar to PMH. Finally, incorporation of acetate into intracellular-free cholesterol was comparable for all cells to PMH; however, insulin-stimulated glucose conversion into lipids and the incorporation of acetate into intracellular cholesterol esters were strikingly different between PMHs and all tested cell lines. In general, AML12 cells most closely phenocopied PMH in vitro energy metabolism. However, the cell line most representative of PMHs differed depending on the mode of metabolism being investigated, and so careful consideration is needed in model selection.

scholarly journals Atypical antipsychotics alter cholesterol and fatty acid metabolism in vitro

2012 ◽  
Vol 54 (2) ◽  
pp. 310-324 ◽  
Author(s):  
Alberto Canfrán-Duque ◽  
María E. Casado ◽  
Óscar Pastor ◽  
Jana Sánchez-Wandelmer ◽  
Gema de la Peña ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Atypical Antipsychotics ◽  
Acid Metabolism

Free fatty acid metabolism and obesity in man: In vivo in vitro comparisons

Metabolism ◽  
1986 ◽  
Vol 35 (6) ◽  
pp. 505-514 ◽  
Author(s):  
S. Lillioja ◽  
J. Foley ◽  
C. Bogardus ◽  
D. Mott ◽  
B.V. Howard
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Free Fatty Acid Metabolism

In Vitro Studies of Fatty Acid Metabolism in Vitamin B6 Deficient Rats

1979 ◽  
Vol 109 (1) ◽  
pp. 138-141 ◽  
Author(s):  
Pierre E. Dussault ◽  
Marius Lepage
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Vitamin B6 ◽  
Acid Metabolism ◽  
In Vitro Studies

scholarly journals In vitro Silencing of Acetyl-CoA Carboxylase beta (ACACB) Gene Reduces Cholesterol Synthesis in Knockdown Chicken Myoblast Cells

2021 ◽  
Author(s):  
G. Sushma ◽  
P. Jaya Laxmi ◽  
S.T. Viroji Rao ◽  
R.M.V. Prasad ◽  
M. Kanakachari ◽  
...  
Keyword(s):  
Cell Culture ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Culture System ◽  
Acid Metabolism ◽  
Cell Culture System ◽  
Acetyl Coa Carboxylase ◽  
Significant Difference ◽  
Myoblast Cells

Abstract The poultry industry provides cost-effective, healthy, and protein-enriched food for the growing population and achieving the nutritional security to the country. Excessive abdominal and subcutaneous fat deposition is one of the major setbacks to the poultry industry that reduces carcass yield and feed efficiency. In chicken abdominal fat constitutes 20% of total body fat which make up 2–3% of live weight of the bird. In fatty acid metabolism, acetyl-CoA Carboxylase (ACC) is one of the key enzymes with two isoforms i.e. ACACA and ACACB each of which plays a different role. In chicken, ACACB is involved in the β-oxidation of fatty acids and thereby potentially regulating the quality of meat and egg. The RNAi strategy is widely used for silencing the target gene expression. In this study, we designed five shRNA constructs and identified the most efficient shRNA molecule for silencing the ACACB gene under in vitro chicken embryo myoblast (CEM) primary cell culture system. After knocking down the ACACB gene, for understanding how fatty acid metabolism is regulated, we tracked the expression of key fatty acid metabolism genes like ACACA, FASN, SCD, ELOVL2, and CPT1. Also, checked the expression of immune response genes like IFNA, IFNB, and BLB1 in control as well as ACACB knockdown myoblast cells and observed no significant difference. We observed the down-regulation of key fatty acid metabolism genes along with ACACB, which may leads to the less fat accumulation in CEM cells. We also estimated the cholesterol and triglycerides in control and ACACB knockdown myoblast cells and found a significant difference between control and the knockdown cells. In vitro knockdown of the ACACB gene in a cell culture system by a short hairpin RNA (shRNA) expressing construct would help to produce a knockdown chicken with reduced fat deposition.

scholarly journals Metabolomics-Based Biomarkers for Frailty in Chinese Older Adults

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 534-534
Author(s):  
Yiming Pan ◽  
Pan Liu ◽  
Yun Li ◽  
Lina Ma
Keyword(s):  
Older Adults ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Fatty Acid Metabolism ◽  
Unsaturated Fatty Acid ◽  
Acid Metabolism ◽  
Untargeted Metabolomics ◽  
Clinical State ◽  
Citrate Cycle ◽  
Chinese Older Adults

Abstract Background Frailty is a clinical state characterized by decline in physiological function, and increased vulnerability to adverse outcomes. The biological mechanisms underlying frailty have been extensively studied in recent years. Advances in the multi-omics platforms have provided new information on the molecular mechanisms of frailty. Thus, identifying omics-based biomarkers is helpful for both exploring the physiological mechanisms of frailty and evaluating the risk of frailty development and progression. Objective To identify metabolomics biomarkers and possible pathogenic mechanisms for frailty with untargeted-metabolomics profiling. Methods LC-MS-based untargeted metabolomics analysis was performed on serum samples of 25 frail older inpatients and 49 non-frail older controls. The metabolomics profiling was compared between the two groups. Results We identified 349 metabolites belonging to 46 classes, in which 2 were increased and 3 were decreased in frail older adults. Citrate cycle (with up-regulated cis-Aconitic acid, Fumaric acid, L-Malic acid, and Isocitric acid), fatty acid metabolism (with up-regulated Palmitic acid and L-Palmitoylcarnitine) and tryptophan metabolism (with up-regulated 5-Hydroxy-L-tryptophan, L-Kynurenine, Kynurenic acid, and 5-Hydroxyindoleacetic acid) were significantly associated with frailty phenotype. Conclusions Our results revealed characteristics of metabolites of frailty in Chinese older adults. The citrate cycle related metabolites (Isocitrate, (s)-Malate, Fumarate and cis-Aconitate), saturated fat (Palmitic acid), unsaturated fatty acid (Arachidonate and Linoleic acid), and some essential amino acid (Tryptophan) might be candidate biomarkers for early diagnosis of frailty. Disorders of energy metabolism, lipotoxicity of saturated fatty acids, disturbances of unsaturated fatty acid metabolism, and increased degradation of tryptophan were potential mechanisms and therapeutic targets of frailty.

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