scholarly journals Spatiotemporal dynamics of triglyceride storage in unilocular adipocytes

2014 ◽  
Vol 25 (25) ◽  
pp. 4096-4105 ◽  
Author(s):  
Michael Chu ◽  
Harini Sampath ◽  
David Y. Cahana ◽  
Christoph A. Kahl ◽  
Romel Somwar ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Endoplasmic Reticulum ◽  
Adipose Tissue ◽  
Free Fatty Acids ◽  
Lipid Droplets ◽  
Ex Vivo ◽  
Spatiotemporal Dynamics ◽  
Biological Features ◽  
Adipocyte Hypertrophy ◽  
Cellular Organelles

The spatiotemporal dynamics of triglyceride (TG) storage in unilocular adipocytes are not well understood. Here we applied ex vivo technology to study trafficking and metabolism of fluorescent fatty acids in adipose tissue explants. Live imaging revealed multiple cytoplasmic nodules surrounding the large central lipid droplet (cLD) of unilocular adipocytes. Each cytoplasmic nodule harbors a series of closely associated cellular organelles, including micro–lipid droplets (mLDs), mitochondria, and the endoplasmic reticulum. Exogenously added free fatty acids are rapidly adsorbed by mLDs and concurrently get esterified to TG. This process is greatly accelerated by insulin. mLDs transfer their content to the cLD, serving as intermediates that mediate packaging of newly synthesized TG in the large interior of a unilocular adipocyte. This study reveals novel cell biological features that may contribute to the mechanism of adipocyte hypertrophy.

scholarly journals The Perfect Storm: Obesity, Adipocyte Dysfunction, and Metabolic Consequences

2008 ◽  
Vol 54 (6) ◽  
pp. 945-955 ◽  
Author(s):  
Sarah de Ferranti ◽  
Dariush Mozaffarian
Keyword(s):  
Fatty Acids ◽  
Endoplasmic Reticulum ◽  
Free Fatty Acids ◽  
Health Effects ◽  
Inflammatory Mediators ◽  
Laboratory Evaluation ◽  
Energy Imbalance ◽  
Adverse Health Effects ◽  
Adverse Health ◽  
Adipocyte Hypertrophy

Abstract Background: As the prevalence of adiposity soars in both developed and developing nations, appreciation of the close links between obesity and disease increases. The strong relationships between excess adipose tissue and poor health outcomes, including cardiovascular disease, diabetes, and cancer, mandate elucidation of the complex cellular, hormonal, and molecular pathophysiology whereby adiposity initiates and maintains adverse health effects. Content: In this report we review adipocyte metabolism and function in the context of energy imbalance and postprandial nutrient excess, including adipocyte hypertrophy and hyperplasia, adipocyte dysfunction, and other systemic consequences. We also discuss implications for laboratory evaluation and clinical care, including the role of lifestyle modifications. Chronic energy imbalance produces adipocyte hypertrophy and hyperplasia, endoplasmic reticulum stress, and mitochondrial dysfunction. These processes lead to increased intracellular and systemic release of adipokines, free fatty acids, and inflammatory mediators that cause adipocyte dysfunction and induce adverse effects in the liver, pancreatic β-cells, and skeletal muscle as well as the heart and vascular beds. Several specialized laboratory tests can quantify these processes and predict clinical risk, but translation to the clinical setting is premature. Current and future pharmacologic interventions may target these pathways; modest changes in diet, physical activity, weight, and smoking are likely to have the greatest impact. Summary: Adipocyte endoplasmic reticulum and mitochondrial stress, and associated changes in circulating adipokines, free fatty acids, and inflammatory mediators, are central to adverse health effects of adiposity. Future investigation should focus on these pathways and on reversing the adverse lifestyle behaviors that are the fundamental causes of adiposity.

The Relationship of Fasting Free Fatty Acids, Adipose Tissue, Insulin Resistance, and Fasting Glucose Concentrations with Subsequent ß-Cell Function in Nondiabetic Subjects

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1812-P
Author(s):  
MARIA D. HURTADO ◽  
J.D. ADAMS ◽  
MARCELLO C. LAURENTI ◽  
CHIARA DALLA MAN ◽  
CLAUDIO COBELLI ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Free Fatty Acids ◽  
Cell Function ◽  
Fasting Glucose ◽  
Relationship Of ◽  
The Relationship

scholarly journals Release of free fatty acids from adipose tissue obtained from newborn infants

1965 ◽  
Vol 6 (1) ◽  
pp. 91-95
Author(s):  
Milan Novák ◽  
Václav Melichar ◽  
Petr Hahn ◽  
Otakar Koldovský
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Free Fatty Acids ◽  
Newborn Infants

Fat Metabolism in Heavy Exercise

1980 ◽  
Vol 59 (6) ◽  
pp. 469-478 ◽  
Author(s):  
N. L. Jones ◽  
G. J. F. Heigenhauser ◽  
A. Kuksis ◽  
C. G. Matsos ◽  
J. R. Sutton ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Free Fatty Acids ◽  
Respiratory Exchange Ratio ◽  
Fat Metabolism ◽  
Maximum Power ◽  
Oxygen Intake ◽  
Heavy Exercise ◽  
Heavy Work ◽  
Adipose Tissue Lipolysis

1. To investigate differences between the metabolic effects of light and heavy exercise, five healthy males (mean maximal oxygen intake 3.92 litres/min) exercised for 40 min at 36% maximum power (light work) and 70% maximum power (heavy work) on separate days, after an overnight fast. 2. A steady state was achieved in both studies between 20 and 40 min in: oxygen intake (1.42 and 2.64 litres/min respectively); respiratory exchange ratio (0.89 and 1.01); plasma lactate concentration (1.78 and 9.94 mmol/l). 3. Plasma palmitate turnover rate (14C) was unchanged from resting values in light work but was decreased by 40% (from 104 ± 16 to 63 ± 8 μmol/min) in heavy work. Heavy work was associated with falls in the plasma concentrations of all free fatty acids measured: palmitic acid (C16:0), oleic acid (C18:1), stearic acid (C18:0), linoleic acid (C18:2) and palmitoleic acid (C16:1). 4. In contrast to the fall in palmitate turnover the increase in plasma glycerol was greater in heavy exercise (0.054–0.229 mmol/l) than in light exercise (0.053–0.094 mmol/l), suggesting that lipolysis was occurring which did not lead to influx of free fatty acids into plasma. 5. In light exercise fat metabolism may be controlled to favour adipose tissue lipolysis and extraction of free fatty acids by muscle from the circulation, whereas in heavy exercise adipose tissue lipolysis is inhibited and hydrolysis of muscle triglycerides may play a more important part. 6. The finding of a high respiratory exchange ratio may not exclude the use of fat as a major fuel source in exercise associated with lactate production.

scholarly journals Mdm1 maintains endoplasmic reticulum homeostasis by spatially regulating lipid droplet biogenesis

2019 ◽  
Vol 218 (4) ◽  
pp. 1319-1334 ◽  
Author(s):  
Hanaa Hariri ◽  
Natalie Speer ◽  
Jade Bowerman ◽  
Sean Rogers ◽  
Gang Fu ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Endoplasmic Reticulum ◽  
Lipid Droplet ◽  
Lipid Droplets ◽  
Fatty Acyl ◽  
Nutrient Depletion ◽  
Coenzyme A Ligase ◽  
Response To Stress ◽  
Acyl Coenzyme A ◽  
Er Homeostasis

Lipid droplets (LDs) serve as cytoplasmic reservoirs for energy-rich fatty acids (FAs) stored in the form of triacylglycerides (TAGs). During nutrient stress, yeast LDs cluster adjacent to the vacuole/lysosome, but how this LD accumulation is coordinated remains poorly understood. The ER protein Mdm1 is a molecular tether that plays a role in clustering LDs during nutrient depletion, but its mechanism of function remains unknown. Here, we show that Mdm1 associates with LDs through its hydrophobic N-terminal region, which is sufficient to demarcate sites for LD budding. Mdm1 binds FAs via its Phox-associated domain and coenriches with fatty acyl–coenzyme A ligase Faa1 at LD bud sites. Consistent with this, loss of MDM1 perturbs free FA activation and Dga1-dependent synthesis of TAGs, elevating the cellular FA level, which perturbs ER morphology and sensitizes yeast to FA-induced lipotoxicity. We propose that Mdm1 coordinates FA activation adjacent to the vacuole to promote LD production in response to stress, thus maintaining ER homeostasis.

Adipose tissue in experimental nephrotic syndrome

1963 ◽  
Vol 205 (4) ◽  
pp. 702-706 ◽  
Author(s):  
Alisa Gutman ◽  
Eleazar Shafrir
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Nephrotic Syndrome ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Lipoprotein Lipase ◽  
Epididymal Adipose Tissue ◽  
Adequate Nutrition ◽  
Defective Metabolism ◽  
Inadequate Food Intake

Epididymal adipose tissue of aminonucleoside-treated rats, investigated 3 to 6 days after induction of the nephrotic syndrome, had low glycogen levels and showed impaired esterification of free fatty acids and assimilation of lipoprotein triglyceride and markedly reduced liberation of lipoprotein lipase. These results were found to be influenced by the inadequate food intake of the acutely nephrotic animals and comparable to the values of control rats fasted for 2 days. On return to adequate nutrition, which occurred 12–20 days after aminonucleoside treatment, adipose tissue glycogen and free fatty acid assimilation returned toward normal levels but lipoprotein-lipase liberation remained below normal. In rats rendered nephrotic by antikidney serum, the assimilation of free fatty acids and lipoprotein-triglyceride by adipose tissue was impaired in spite of only minor reduction in food consumption. The results indicate that the defective metabolism of adipose tissue in nephrotic animals may be contributory to the nephrotic hypertriglyceridemia.

Effect of exercise on hormone-sensitive lipase activity in rat adipocytes

1976 ◽  
Vol 230 (2) ◽  
pp. 385-388 ◽  
Author(s):  
JA McGarr ◽  
LB Oscai ◽  
J Borensztajn
Keyword(s):  
Fatty Acids ◽  
Enzyme Activity ◽  
Adipose Tissue ◽  
Free Fatty Acids ◽  
Lipase Activity ◽  
Exercise Program ◽  
Treadmill Running ◽  
Hormone Sensitive Lipase ◽  
Hormone Sensitive ◽  
Fat Pads

Hormone-sensitive lipase activity was measured in adipocytes of rats subjected to a 12-wk program of treadmill running. Enzyme activity in the runners sacrificed immediately after exercise increased 2.5-fold (P less than 0.001) in tissue exposed to epinephrine and threefold (P less than 0.001) in tissue not exposed to epinephrine, when the results were expressed per gram of adipose tissue. Increases of almost the same magnitude were observed in runners sacrificed 24 h after their last bout of work. These significant increases in enzyme activity, however, were the result of a significant reduction in the size of cells in the epididymal fat pads of the exercisers compared with those of the freely eating sedentary animals (68.7 +/- 2.7 mum vs. 82.0 +/- 2.7 mum; P less than 0.01). When the results were expressed on a per-cell basis, therefore, hormone-sensitive lipase activity, assayed in the presence or absence of epinephrine, was unaffected by the exercise program. These results provide evidence that the lipolytic capacity of adipocytes of normal, untrained rats is sufficiently large to meet the increased demand for free fatty acids imposed by the exercise program without the need for an adaptive increase in enzyme activity.

Sign in / Sign up

Export Citation Format

Share Document