Effect of aging on lipid composition and metabolism in the adipose tissues of the rat

1961 ◽  
Vol 201 (3) ◽  
pp. 540-546 ◽  
Author(s):  
William Benjamin ◽  
Alfred Gellhorn ◽  
Mary Wagner ◽  
Harold Kundel
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Palmitic Acid ◽  
Subcutaneous Fat ◽  
Lipid Synthesis ◽  
Pentose Phosphate ◽  
Acid Oxidation ◽  
Acetate Incorporation ◽  
Adipose Tissues

Lipid metabolism and chemistry was studied in adipose tissues of the rat from the age of 38 days to 647 days. Aging process was characterized by a marked decrease in lipid synthesis from acetate, a reduction in the proportion of glucose metabolized by the pentose phosphate pathway, and a lower rate of palmitate incorporation into the mixed lipids. Oxidation of palmitic acid to CO2 and release of free fatty acid by epididymal fat was the same in young and old tissues under control conditions; when, however, glucose was absent from the medium or when epinephrine was added, there was a significantly greater rate of palmitic acid oxidation and free fatty acid release by young compared to old adipose tissue. Rate of acetate incorporation into mixed lipids by multiple adipose tissue sites was determined at different ages. Consistently greater rates of lipid biosynthesis were found in the epididymal, perirenal, mesenteric and interscapular adipose tissues than in subcutaneous fat at all ages. Rate of lipid synthesis by the interscapular fat (unlike any of the other depots) remained high at all ages studied. A greater proportion of short chain fatty acids was found in adipose tissues from young rats than in the old. This was related to fatty acid composition of rat milk.

Influence of Free Fatty Acid Concentrations and Weight Loss on Adipose Tissue Direct Free Fatty Acid Storage Rates

2021 ◽  
Author(s):  
Qingyi Jia ◽  
B Gisella Carranza Leon ◽  
Michael D Jensen
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Subcutaneous Fat ◽  
Premenopausal Women ◽  
Tissue Level ◽  
Research Unit ◽  
Lower Body ◽  
Plasma Ffa

Abstract Context The factors that determine the recycling of free fatty acids (FFA) back into different adipose tissue depots via the direct storage pathway are not completely understood. Objective To assess the interactions between adipocyte factors and plasma FFA concentrations that determine regional FFA storage rates. Design We measured direct adipose tissue FFA storage rates before and after weight loss under high FFA (intravenous somatostatin and epinephrine) and low (intravenous insulin and glucose) FFA concentrations. Setting Mayo Clinic Clinical Research Unit. Patients Sixteen premenopausal women, BMI 30 - 37 kg/m 2. Intervention Comprehensive lifestyle weight loss program. Main Outcome Measure Direct FFA storage rates in upper and lower body subcutaneous fat. Results Over the entire range of FFA and under isolated conditions of elevated FFA concentrations the storage rates of FFA into upper and lower body subcutaneous fat per unit lipid were associated with concentrations, not adipocyte fatty acid storage factors. Under low FFA conditions, direct FFA storage rates were related to adipocyte CD36 content, not tissue level content of fatty acid storage factors. Weight loss did not change these relationships. Conclusions The regulation of direct FFA storage under low FFA concentration conditions appears to be at the level of the cell/adipocyte content of CD36, whereas under high FFA concentration conditions direct FFA storage at the tissue level is predicted by plasma FFA concentrations, independent of adipocyte size or fatty acid storage factors. These observations offer novel insights into how adipose tissue regulates direct FFA storage in humans.

scholarly journals Clearing-factor lipase in muscle and adipose tissue of pigs

1973 ◽  
Vol 136 (2) ◽  
pp. 381-385 ◽  
Author(s):  
M. Enser
Keyword(s):  
Enzyme Activity ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Plasma Insulin ◽  
Subcutaneous Fat ◽  
Rapid Decrease ◽  
Plasma Fatty Acid ◽  
Plasma Insulin Concentration ◽  
Adipose Tissues ◽  
Perirenal Fat

1. Clearing-factor lipase was assayed in acetone–ether-dried powders of heart and adipose tissue of pigs. The enzyme activity in heart was higher than that in adipose tissue. The activity in the outer layer of subcutaneous fat was greater than that in the inner subcutaneous fat and the perirenal fat, which had similar activities. 2. Starvation for 48h, but not for 24h, decreased the activity of the heart enzyme. 3. Starvation for 24h caused a rapid decrease in the activity in all three adipose tissues, but even after 72h of starvation the activity was still highest in the outer subcutaneous fat. 4. Plasma fatty acid, glucose and insulin concentrations were determined in fed and starved pigs. Starvation decreased the plasma insulin concentration and increased the non-esterified fatty acid concentration.

scholarly journals Chronic cold exposure induces autophagy to promote fatty acid oxidation, mitochondrial turnover, and thermogenesis in brown adipose tissue

iScience ◽  
2021 ◽  
pp. 102434
Author(s):  
Winifred W. Yau ◽  
Kiraely Adam Wong ◽  
Jin Zhou ◽  
Nivetha Kanakaram Thimmukonda ◽  
Yajun Wu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Fatty Acid Oxidation ◽  
Cold Exposure ◽  
Acid Oxidation ◽  
Brown Adipose ◽  
Mitochondrial Turnover

scholarly journals miR-21-5p regulates mitochondrial respiration and lipid content in H9C2 cells

2019 ◽  
Vol 316 (3) ◽  
pp. H710-H721 ◽  
Author(s):  
Victoria L. Nasci ◽  
Sandra Chuppa ◽  
Lindsey Griswold ◽  
Kathryn A. Goodreau ◽  
Ranjan K. Dash ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Fatty Acid Oxidation ◽  
Lipid Content ◽  
Mitochondrial Respiration ◽  
Acid Oxidation ◽  
H9c2 Cells ◽  
Cellular Lipid ◽  
Transfected Cells

Cardiovascular-related pathologies are the single leading cause of death in patients with chronic kidney disease (CKD). Previously, we found that a 5/6th nephrectomy model of CKD leads to an upregulation of miR-21-5p in the left ventricle, targeting peroxisome proliferator-activated receptor-α and altering the expression of numerous transcripts involved with fatty acid oxidation and glycolysis. In the present study, we evaluated the potential for knockdown or overexpression of miR-21-5p to regulate lipid content, lipid peroxidation, and mitochondrial respiration in H9C2 cells. Cells were transfected with anti-miR-21-5p (40 nM), pre-miR-21-5p (20 nM), or the appropriate scrambled oligonucleotide controls before lipid treatment in culture or as part of the Agilent Seahorse XF fatty acid oxidation assay. Overexpression of miR-21-5p attenuated the lipid-induced increase in cellular lipid content, whereas suppression of miR-21-5p augmented it. The abundance of malondialdehyde, a product of lipid peroxidation, was significantly increased with lipid treatment in control cells but attenuated in pre-miR-21-5p-transfected cells. This suggests that miR-21-5p reduces oxidative stress. The cellular oxygen consumption rate (OCR) was increased in both pre-miR-21-5p- and anti-miR-21-5p-transfected cells. Levels of intracellular ATP were significantly higher in anti-mR-21-5p-transfected cells. Pre-miR-21-5p blocked additional increases in OCR in response to etomoxir and palmitic acid. Conversely, anti-miR-21-5p-transfected cells exhibited reduced OCR with both etomoxir and palmitic acid, and the glycolytic capacity was concomitantly reduced. Together, these results indicate that overexpression of miR-21-5p attenuates both lipid content and lipid peroxidation in H9C2 cells. This likely occurs by reducing cellular lipid uptake and utilization, shifting cellular metabolism toward reliance on the glycolytic pathway. NEW & NOTEWORTHY Both overexpression and suppression of miR-21-5p augment basal and maximal mitochondrial respiration. Our data suggest that reliance on glycolytic and fatty acid oxidation pathways can be modulated by the abundance of miR-21-5p within the cell. miR-21-5p regulation of mitochondrial respiration can be modulated by extracellular lipids.

scholarly journals Modulation of lipid-synthesizing enzymes by insulin in differentiated ob17 adipose-like cells

1983 ◽  
Vol 214 (2) ◽  
pp. 443-449 ◽  
Author(s):  
P Grimaldi ◽  
C Forest ◽  
P Poli ◽  
R Negrel ◽  
G Ailhaud
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Specific Activity ◽  
Fatty Acid Synthetase ◽  
Lipid Synthesis ◽  
Acid Synthesis ◽  
Acetate Incorporation ◽  
Long Term Effects ◽  
Response Curves ◽  
Glycerol 3 Phosphate Dehydrogenase

ob17 cells convert into adipose-like cells when maintained in the presence of physiological concentrations of insulin and tri-iodothyronine. After this conversion, insulin removal from differentiated ob17 cells gives within 24-48 h a large decrease in fatty acid synthetase, glycerol 3-phosphate dehydrogenase and acid:CoA ligase activities, as well as in the rate of fatty acid synthesis determined by [14C]acetate incorporation into lipids. All parameters are restored by insulin addition to initial values within 24-48 h. Dose-response curves of insulin on the restoration of glycerol 3-phosphate dehydrogenase activity and of fatty acid synthesis give half-maximally effective concentrations close to 1 nM, in agreement with the affinity for insulin of the insulin receptors previously characterized in these cells. Immunotitration experiments indicate that the changes in the specific activity of fatty acid synthetase are due to parallel changes in the cellular enzyme content. Therefore the ob17 cell line should be a useful model to study the long-term effects of insulin on the modulation of lipid synthesis in adipose cells.

scholarly journals Clearing-factor lipase in adipose tissue. A possible role of adenosine 3′,5′-(cyclic)-monophosphate in the regulation of its activity

1968 ◽  
Vol 109 (5) ◽  
pp. 841-849 ◽  
Author(s):  
D. R. Wing ◽  
D S Robinson
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Cyclic Amp ◽  
Lipase Activity ◽  
Glucose Concentration ◽  
Free Fatty Acid Concentration ◽  
Epididymal Fat ◽  
Fat Bodies

1. The rise in clearing-factor lipase activity that occurs when epididymal fat bodies from starved rats are incubated in appropriate media in vitro is inhibited in the presence of 6-N-2′-O-dibutyryl-3′,5′-(cyclic)-AMP (1mm). 2. Inhibition occurs at a concentration of glucose in the incubation medium of 1·3mg./ml. or less, but not at a glucose concentration of 2·4mg./ml., unless caffeine (1mm), an inhibitor of 3′,5′-(cyclic)-nucleotide phosphodiesterase, is also present. Caffeine (5mm) alone inhibits the rise in clearing-factor lipase activity at a glucose concentration of 2·4mg./ml. of medium. 3. The concentration of free fatty acids in the epididymal fat bodies normally falls during incubations in vitro as the rise in clearing-factor lipase activity occurs. In the presence of 1mm-6-N-2′-O-dibutyryl-3′,5′-(cyclic)-AMP, however, either the tissue free fatty acid concentration is increased or it does not fall to the same extent. The concentration of glucose in the incubation medium is important in determining the direction and extent of the changes in tissue free fatty acid concentration that occur in the presence of 6-N-2′-O-dibutyryl-3′,5′-(cyclic)-AMP. 4. Free fatty acid concentrations in epididymal fat bodies in vivo rise as the clearing-factor lipase activity of the tissue falls during starvation. 5. The possibility that the concentration of 3′,5′-(cyclic)-AMP in adipose tissue may regulate clearing-factor lipase activity, and that the regulation may occur through effects of the nucleotide on tissue free fatty acid concentrations, is discussed.

scholarly journals Stimulation of Mitochondrial Fatty Acid Oxidation by Growth Hormone in Human Fibroblasts1

1997 ◽  
Vol 82 (12) ◽  
pp. 4208-4213 ◽  
Author(s):  
Kin-Chuen Leung ◽  
Ken K. Y. Ho
Keyword(s):  
Fatty Acid ◽  
Growth Factor ◽  
Lipid Oxidation ◽  
Palmitic Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
Growth Factor I ◽  
Stimulation Of

In vivo administration of GH induces lipolysis and lipid oxidation. However, it is not clear whether the stimulation of lipid oxidation is a direct effect of GH or is driven by increased substrate supply secondary to lipolysis. An in vitro bioassay has been established for assessing β-oxidation of fatty acids in mitochondria, based on the measurement of conversion of tritiated palmitic acid to 3H2O by fibroblasts in culture. We have modified this assay to investigate whether GH stimulates fatty acid oxidation. GH stimulated oxidation of palmitic acid maximally by 26.7 ± 2.5% (mean ± sem; P < 0.0001). The stimulation was biphasic, with the oxidation rate increasing with increasing GH concentration to a peak response at 1.5 nmol/L and declining to a level not significantly different from control thereafter. Insulin-like growth factor-I at concentrations of up to 250 nmol/L had no significant effect on fatty acid oxidation. GH-binding protein attenuated the effect of GH. An anti-GH receptor (GHR) antibody (MAb263), which dimerizes the receptor and induces GH-like biological actions, significantly stimulated fatty acid oxidation. Another anti-GHR antibody (MAb5), which prevents receptor dimerization, suppressed GH action. In summary, GH directly stimulated fatty acid oxidation, an action not mediated by insulin-like growth factor-I. Dimerization of GHRs was necessary for this effect. This bioassay is a practical tool for studying the regulatory effects of GH on lipid oxidation.

Isotope tracer measures of meal fatty acid metabolism: reproducibility and effects of the menstrual cycle

2005 ◽  
Vol 288 (3) ◽  
pp. E547-E555 ◽  
Author(s):  
Ana Paola Uranga ◽  
James Levine ◽  
Michael Jensen
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Menstrual Cycle ◽  
Dietary Fat ◽  
Fatty Acid Uptake ◽  
Upper Body ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Lower Body

Oxidation and adipose tissue uptake of dietary fat can be measured by adding fatty acid tracers to meals. These studies were conducted to measure between-study variability of these types of experiments and assess whether dietary fatty acids are handled differently in the follicular vs. luteal phase of the menstrual cycle. Healthy normal-weight men ( n = 12) and women ( n = 12) participated in these studies, which were block randomized to control for study order, isotope ([3H]triolein vs. [14C]triolein), and menstrual cycle. Energy expenditure (indirect calorimetry), meal fatty acid oxidation, and meal fatty acid uptake into upper body and lower body subcutaneous fat (biopsies) 24 h after the experimental meal were measured. A greater portion of meal fatty acids was stored in upper body subcutaneous adipose tissue (24 ± 2 vs. 16 ± 2%, P < 0.005) and lower body fat (12 ± 1 vs. 7 ± 1%, P < 0.005) in women than in men. Meal fatty acid oxidation (3H2O generation) was greater in men than in women (52 ± 3 vs. 45 ± 2%, P = 0.04). Leg adipose tissue uptake of meal fatty acids was 15 ± 2% in the follicular phase of the menstrual cycle and 10 ± 1% in the luteal phase ( P = NS). Variance in meal fatty acid uptake was somewhat ( P = NS) greater in women than in men, although menstrual cycle factors did not contribute significantly. We conclude that leg uptake of dietary fat is slightly more variable in women than in men, but that there are no major effects of menstrual cycle on meal fatty acid disposal.

scholarly journals Cellular retinol-binding protein type III is a PPARγ target gene and plays a role in lipid metabolism

2008 ◽  
Vol 295 (6) ◽  
pp. E1358-E1368 ◽  
Author(s):  
Cynthia F. Zizola ◽  
Gary J. Schwartz ◽  
Silke Vogel
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Free Fatty Acid ◽  
Target Gene ◽  
Binding Protein ◽  
Retinol Binding Protein ◽  
Wild Type ◽  
Type Iii ◽  
Cellular Retinol Binding Protein

Cellular retinol-binding protein (CRBP) type III (CRBP-III) belongs to the family of intracellular lipid-binding proteins, which includes the adipocyte-binding protein aP2. In the cytosol, CRBP-III binds retinol, the precursor of retinyl ester and the active metabolite retinoic acid. The goal of the present work is to understand the regulation of CRBP-III expression and its role in lipid metabolism. Using EMSAs, luciferase reporter assays, and chromatin immunoprecipitation assays, we found that CRBP-III is a direct target of peroxisome proliferator-activated receptor-γ (PPARγ). Moreover, CRBP-III expression was induced in adipose tissue of mice after treatment with the PPARγ agonist rosiglitazone. To examine a potential role of CRBP-III in regulating lipid metabolism in vivo, CRBP-III-deficient (C-III-KO) mice were maintained on a high-fat diet (HFD). Hepatic steatosis was decreased in HFD-fed C-III-KO compared with HFD-fed wild-type mice. These differences were partly explained by decreased serum free fatty acid levels and decreased free fatty acid efflux from adipose tissue of C-III-KO mice. In addition, the lack of CRBP-III was associated with reduced food intake, increased respiratory energy ratio, and altered body composition, with decreased adiposity and increased lean body mass. Furthermore, expression of genes involved in mitochondrial fatty acid oxidation in brown adipose tissue was increased in C-III-KO mice, and C-III-KO mice were more cold tolerant than wild-type mice fed an HFD. In summary, we demonstrate that CRBP-III is a PPARγ target gene and plays a role in lipid and whole body energy metabolism.

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