scholarly journals β-Lactoglobulin-linoleate complexes: In vitro digestion and the role of protein in fatty acid uptake

2013 ◽  
Vol 96 (7) ◽  
pp. 4258-4268 ◽  
Author(s):  
Solène Le Maux ◽  
André Brodkorb ◽  
Thomas Croguennec ◽  
Alan A. Hennessy ◽  
Saïd Bouhallab ◽  
...  
Keyword(s):  
Fatty Acid ◽  
In Vitro Digestion ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Β Lactoglobulin

Palmitic acid uptake by the rat soleus muscle in vitro

2001 ◽  
Vol 79 (4) ◽  
pp. 419-424 ◽  
Author(s):  
M Górecka ◽  
M Synak ◽  
L Budohoski ◽  
J Langfort ◽  
S Moskalewski ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Soleus Muscle ◽  
Fatty Acid Uptake ◽  
Cellular Fatty Acid ◽  
Acid Uptake ◽  
Acid Complex ◽  
Rat Soleus Muscle

The rate of fatty acid uptake, oxidation, and deposition in skeletal muscles in relation to total and unbound to albumin fatty acids concentration in the medium were investigated in the incubated rat soleus muscle. An immunohistochemical technique was applied to demonstrate whether the albumin-bound fatty acid complex from the medium penetrates well within all areas of the muscle strips. It was found that the percentage of incorporation of palmitic acid into intramuscular lipids was fairly constant, independently of the fatty acid concentration in the medium, and amounted to 63–72% for triacylglycerols, 7–12% for diacylglycerols-monoacylglycerols, and 19–26% for phospholipids. Both palmitic acid incorporation into the muscle triacylglycerol stores and its oxidation to CO2closely correlated with an increase in both total and unbound to albumin fatty acid concentrations in the incubation medium. Under conditions of increased total but constant unbound to albumin palmitic acid concentrations, the incorporation of palmitic acid into triacylglycerols and its oxidation to CO2were also increased, but to a lower extent. This supports the hypothesis that the cellular fatty acid metabolism depends not only on the availability of fatty acids unbound to albumin, but also on the availability of fatty acids complexed to albumin.Key words: skeletal muscle, fatty acids, triacylglycerols, phospholipids.

scholarly journals The role of mitochondria linked fatty-acid uptake-driven adipogenesis in Graves’ Orbitopathy

Endocrinology ◽  
2021 ◽  
Author(s):  
Lei Zhang ◽  
Pavandeep Rai ◽  
Satomi Miwa ◽  
Mohd Shazli Draman ◽  
D Aled Rees ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Culture Medium ◽  
Fatty Acid Uptake ◽  
Therapeutic Interventions ◽  
Acid Uptake ◽  
Atp Production ◽  
Oligomycin A ◽  
Graves Orbitopathy

Abstract Context Depot-specific expansion of orbital-adipose-tissue (OAT) in Graves’ Orbitopathy (GO, an autoimmune condition producing proptosis, visual impairment and reduced quality of life) is associated with fatty-acid (FA) uptake-driven adipogenesis in preadipocytes/fibroblasts (PFs). Objective A role for mitochondria in OAT-adipogenesis in GO. Design, Setting, Participants Confluent PFs from healthy OAT (OAT-H), OAT from GO (OAT-GO) and white-adipose-tissue in culture-medium compared with culture-medium containing a mixed hormonal-cocktail as adipogenic-medium (ADM); or culture-medium containing FA-supplementation, oleate:palmitate:linoleate (45:30:25%) with/without different concentration of mitochondrial bio-substrate ADP/GDP, AICAR (adenosine-analog) or inhibitor oligomycin-A for 17 days. Main outcome measures Oil-Red-O staining and foci-count of differentiated adipocytes for in-vitro adipogenesis; flow-cytometry, relative-QPCR, MTS-assay/10 6 cells, total cellular-ATP detection kit and Seahorse-XFe96-Analyzer for mitochondria and OXPHOS/Glycolysis-ATP production analysis. Results During early adipogenesis before adipocyte formation (day-0,4&7), we observed OAT-specific cellular ATP-production via mitochondrial-OXPHOS in PFs from both OAT-H/OAT-GO, and substantially disrupted OXPHOS-ATP/Glycolysis-ATP production in PFs from OAT-GO, e.g. 40% reduction in OXPHOS-ATP and trend-increased Glycolysis-ATP production on day-4&7 compared with day-0, which contrasted with the stable levels in OAT-H.FA-supplementation in culture-medium triggered adipogenesis in PFs from both OAT-H/OAT-GO, which was substantially enhanced by 1mM GDP reaching 7-18% of ADM-adipogenesis. The FA-uptake-driven adipogenesis was diminished by oligomycin-A but unaffected by treatment with ADP or AICAR. Furthermore, we observed significant positive correlation between FA-uptake-driven adipogenesis by GDP and the ratios of OXPHOS-ATP/Glycolysis-ATP through adipogenesis of PFs from OAT-GO. Conclusions Our study confirmed that FA-uptake can drive OAT-adipogenesis and revealed a fundamental role for mitochondria-OXPHOS in GO development, which provides potential for therapeutic interventions.

Theobromine ameliorates nonalcoholic fatty liver disease by regulating hepatic lipid metabolism via mTOR signaling pathway in vivo and in vitro

2020 ◽  
Author(s):  
Dan Wei ◽  
Shaofei Wu ◽  
Jie Liu ◽  
Xiaoqian Zhang ◽  
Xiaoling Guan ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Signaling Pathway ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Uptake ◽  
Mtor Signaling ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Mtor Signaling Pathway

Theobromine, a methylxanthine present in cocoa, has been shown to possess many beneficial pharmacological properties such as anti-oxidative stress, anti-inflammatory property, and anti-microbial activity. In this study, we investigated the effects of theobromine on NAFLD and the possible underlying mechanisms in vivo and in vitro. The results showed that theobromine reduced body weight, fat mass and improved dyslipidemia. Theobromine decreased liver weight, mitigated liver injury, and significantly reduced hepatic TG level in mice with obesity. Histological examinations also showed hepatic steatosis was alleviated after theobromine treatment. Furthermore, theobromine reversed the elevated mRNA and protein expression of SREBP-1c, FASN, CD36, FABP4 and the suppressed expression of PPARα, CPT1a in the liver of mice with obesity, which were responsible for lipogenesis, fatty acid uptake and fatty acid oxidation respectively. In vitro, theobromine also downregulated SREBP-1c, FASN, CD36, FABP4 and upregulated PPARα, CPT1a mRNA and protein levels in hepatocytes in a dose-dependent manner, while these changes were reversed by L-Leucine, an mTOR agonist. The present study demonstrated that theobromine improved NAFLD by inhibiting lipogenesis, fatty acid uptake and promoting fatty acid oxidation in the liver and hepatocytes, which might be associated with its suppression of mTOR signaling pathway.

scholarly journals In Vivo Optical Metabolic Imaging of Long-Chain Fatty Acid Uptake in Orthotopic Models of Triple-Negative Breast Cancer

Cancers ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 148
Author(s):  
Megan C. Madonna ◽  
Joy E. Duer ◽  
Joyce V. Lee ◽  
Jeremy Williams ◽  
Baris Avsaroglu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Fatty Acid ◽  
Triple Negative ◽  
Fatty Acid Uptake ◽  
Chain Fatty Acid ◽  
Acid Uptake ◽  
Long Chain Fatty Acid ◽  
Long Chain

Targeting a tumor’s metabolic dependencies is a clinically actionable therapeutic approach; however, identifying subtypes of tumors likely to respond remains difficult. The use of lipids as a nutrient source is of particular importance, especially in breast cancer. Imaging techniques offer the opportunity to quantify nutrient use in preclinical tumor models to guide development of new drugs that restrict uptake or utilization of these nutrients. We describe a fast and dynamic approach to image fatty acid uptake in vivo and demonstrate its relevance to study both tumor metabolic reprogramming directly, as well as the effectiveness of drugs targeting lipid metabolism. Specifically, we developed a quantitative optical approach to spatially and longitudinally map the kinetics of long-chain fatty acid uptake in in vivo murine models of breast cancer using a fluorescently labeled palmitate molecule, Bodipy FL c16. We chose intra-vital microscopy of mammary tumor windows to validate our approach in two orthotopic breast cancer models: a MYC-overexpressing, transgenic, triple-negative breast cancer (TNBC) model and a murine model of the 4T1 family. Following injection, Bodipy FL c16 fluorescence increased and reached its maximum after approximately 30 min, with the signal remaining stable during the 30–80 min post-injection period. We used the fluorescence at 60 min (Bodipy60), the mid-point in the plateau region, as a summary parameter to quantify Bodipy FL c16 fluorescence in subsequent experiments. Using our imaging platform, we observed a two- to four-fold decrease in fatty acid uptake in response to the downregulation of the MYC oncogene, consistent with findings from in vitro metabolic assays. In contrast, our imaging studies report an increase in fatty acid uptake with tumor aggressiveness (6NR, 4T07, and 4T1), and uptake was significantly decreased after treatment with a fatty acid transport inhibitor, perphenazine, in both normal mammary pads and in the most aggressive 4T1 tumor model. Our approach fills an important gap between in vitro assays providing rich metabolic information at static time points and imaging approaches visualizing metabolism in whole organs at a reduced resolution.

scholarly journals Exendin-4 alleviates hepatic steatosis by lowering FABP1 and raising FOXA1 expression via the Wnt/-catenin signaling pathway

2021 ◽  
Author(s):  
Olfa Khalifa ◽  
Neyla S. AL-AKl ◽  
Khaoula Errafii ◽  
Abdelilah Arredouani
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Hepg2 Cells ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Fatty Acid Binding ◽  
Alcoholic Fatty Liver ◽  
Glucagon Like Peptide 1 ◽  
Vitro Model

Abstract Non-alcoholic fatty liver disease (NAFLD) is the leading chronic liver disease worldwide. Agonists of the glucagon-like peptide-1 receptor (GLP-1R), currently approved to treat type 2 diabetes, hold promise to improve steatosis and even steatohepatitis. However, due to their pleiotropic effects, the mechanisms underlying their protective effect on NAFLD remain elusive. We aimed to investigate these mechanisms using an in vitro model of steatosis treated with the GLP-1R agonist Exendin-4 (Ex-4). We established steatotic HepG2 cells by incubating HepG2 cells with 400 µM oleic acid (OA) overnight. Further treatment with 200nM Ex-4 for 3 hours significantly reduced the OA-induced lipid accumulation (p < 0.05). Concomitantly, Ex-4 substantially reduced the expression levels of Fatty Acid-Binding Protein 1 (FABP1) and its primary activator, Forkhead box protein A1 (FOXA1). Interestingly, the silencing of β-catenin with siRNA abolished the effect of Ex-4 on these genes, suggesting dependency on the Wnt/β-catenin pathway. Furthermore, after β-catenin silencing, OA treatment significantly increased the expression of nuclear transcription factors SREBP-1 and TCF4, whereas Ex-4 significantly decreased this upregulation. Our findings suggest that direct activation of GLP-1R by Ex-4 reduces OA-induced steatosis in HepG2 cells by reducing fatty acid uptake via FABP1 downregulation.

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