FAT/CD36 regulates PEPCK expression in adipose tissue

2013 ◽  
Vol 304 (5) ◽  
pp. C478-C484 ◽  
Author(s):  
Zhongxiao Wan ◽  
Sarthak Matravadia ◽  
Graham P. Holloway ◽  
David C. Wright
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Mrna Expression ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Fatty Acid Uptake ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Expression Of Genes ◽  
Fatty Acid Release ◽  
Acid Release

Fatty acid translocase (FAT)/CD36 has been extensively studied for its role in facilitating fatty acid uptake. Recent findings have also demonstrated that this protein regulates adipocyte lipolysis and may modulate fatty acid reesterification. As FAT/CD36 has been shown to control the expression of genes involved in fatty acid oxidation in adipocytes, we reasoned that this protein might also control the expression of enzymes involved in fatty acid reesterification. In adipose tissue from FAT/CD36 knockout (KO) mice, we found that glycerol and fatty acid release were reduced and this was associated with reductions in adipose triglyceride lipase. Decreases in lipolysis were paralleled by increases in the free fatty acid-to-glycerol ratio and reductions in primary and fractional rates of fatty acid reesterfication in cultured adipose tissue from FAT/CD36 KO mice. Reductions in reesterfication were associated with decreases in the mRNA expression and protein content of phosphoenolpyruvate carboxykinase (PEPCK). To determine if reductions in lipolysis could lead to decreases in PEPCK mRNA expression, we treated cultured mouse adipose tissue with the lipase inhibitor CAY10499 (2 μM) and found that this resulted in an ∼50% reduction in PEPCK mRNA expression. Treatment with hexarelin (10 μM, 12 h), a CD36 agonist, increased PEPCK mRNA expression independent of lipolysis. Collectively, our results provide novel evidence that FAT/CD36 regulates PEPCK in adipose tissue and that this could be secondary to reductions in lipolysis.

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.

Comparison between Tibetan and Small-tailed Han sheep in adipocyte phenotype, lipid metabolism and energy homoeostasis regulation of adipose tissues when consuming diets of different energy levels

2020 ◽  
Vol 124 (7) ◽  
pp. 668-680
Author(s):  
Xiaoping Jing ◽  
Jianwei Zhou ◽  
Allan Degen ◽  
Wenji Wang ◽  
Yamin Guo ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Energy Balance ◽  
Mrna Expression ◽  
Fatty Acid Uptake ◽  
Negative Energy ◽  
Low Energy ◽  
Harsh Environment ◽  
Acid Uptake ◽  
Tibetan Sheep

AbstractThis study aimed to gain insight into how adipose tissue of Tibetan sheep regulates energy homoeostasis to cope with low energy intake under the harsh environment of the Qinghai-Tibetan Plateau (QTP). We compared Tibetan and Small-tailed Han sheep (n 24 of each breed), all wethers and 1·5 years of age, which were each divided randomly into four groups and offered diets of different digestible energy (DE) densities: 8·21, 9·33, 10·45 and 11·57 MJ DE/kg DM. When the sheep lost body mass and were assumed to be in negative energy balance: (1) adipocyte diameter in subcutaneous adipose tissue was smaller and decreased to a greater extent in Tibetan than in Small-tailed Han sheep, but the opposite occurred in the visceral adipose tissue; (2) Tibetan sheep showed higher insulin receptor mRNA expression and lower concentrations of catabolic hormones than Small-tailed Han sheep and (3) Tibetan sheep had lower capacity for glucose and fatty acid uptake than Small-tailed Han sheep. Moreover, Tibetan sheep had lower AMPKα mRNA expression but higher mammalian target of rapamycin mRNA expression in the adipocytes than Small-tailed Han sheep. We concluded that Tibetan sheep had lower catabolism but higher anabolism in adipose tissue and reduced the capacity for glucose and fatty acid uptake to a greater extent than Small-tailed Han sheep to maintain energy homoeostasis when in negative energy balance. These responses provide Tibetan sheep with a high ability to cope with low energy intake and with the harsh environment of the QTP.

Meal fatty acid uptake in human adipose tissue: technical and experimental design issues

2000 ◽  
Vol 279 (2) ◽  
pp. E447-E454 ◽  
Author(s):  
S. A. Romanski ◽  
Rita M. Nelson ◽  
Michael D. Jensen
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Experimental Design ◽  
Fatty Acid Oxidation ◽  
Fatty Acid Uptake ◽  
Acid Oxidation ◽  
Acid Uptake ◽  
Tissue Uptake ◽  
Design Issues ◽  
Isotopic Tracers

The adipose tissue uptake of dietary fat has been studied using fatty acid radiotracers incorporated into a meal, followed by adipose tissue biopsies. A number of experimental design issues, including the use of isotopic tracers to measure meal fatty acid oxidation and plasma appearance of tracer, as well as the heterogeneity of adipose tissue fatty acid uptake, have been addressed. We examined these questions in a study of 24 volunteers (12 men and 12 women) who consumed a meal containing [3H]triolein and [14C]triolein. Slight differences in the purity of [3H]triolein vs. [14C]triolein were found, which could affect the apparent adipose tissue uptake of meal fatty acids. The adipose tissue triglyceride specific activity from bilateral biopsy sites agreed well, implying that a unilateral biopsy is satisfactory for measuring tracer uptake. Meal fatty acid oxidation measured using [3H]triolein and [14C]triolein was well correlated ( r = 0.79, P < 0.0001). The peak tracer appearance in plasma chylomicrons occurred 1 h after the ingestion of a second, unlabeled meal. Our findings have implications for the experimental design of future meal fatty acid tracer/adipose tissue biopsy studies.

Substance P decreases fat storage and increases adipocytokine production in 3T3-L1 adipocytes

2013 ◽  
Vol 304 (4) ◽  
pp. G420-G427 ◽  
Author(s):  
Pierre Miegueu ◽  
David H. St-Pierre ◽  
Marc Lapointe ◽  
Pegah Poursharifi ◽  
HuiLing Lu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Mrna Expression ◽  
Fatty Acid Uptake ◽  
Complement C3 ◽  
Peroxisome Proliferator ◽  
Acid Uptake ◽  
Peroxisome Proliferator Activated Receptor ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant

Obesity, inflammation, and insulin resistance are closely linked. Substance P (SP), via its neurokinin 1 receptor (NK1R), mediates inflammatory and, possibly, neuroendocrine processes. We examined SP effects on lipid storage and cytokine production in 3T3-L1 adipocytes and adipose tissues. 3T3-L1 adipocytes and preadipocytes express NK1R, and 8 days of SP supplementation during differentiation to 3T3-L1 preadipocytes decreased lipid droplet accumulation. SP (10 nM, 24 h) increased lipolysis in primary adipocytes (138 ± 7%, P < 0.05) and reduced fatty acid uptake (−31 ± 7%, P < 0.05) and mRNA expression of the differentiation-related transcription factors peroxisome proliferator-activated receptor-γ type 2 (−64 ± 2%, P < 0.001) and CCAAT enhancer-binding protein (CEBP)-α (−65 ± 2%, P < 0.001) and the lipid storage genes fatty acid-binding protein type 4 (−59 ± 2%, P < 0.001) and diacylglycerol O-acyltransferase-1 (−45 ± 2%, P < 0.01) in 3T3-L1 adipocytes, while CD36, a fatty acid transporter (+82 ± 19%, P < 0.01), was augmented. SP increased secretion of complement C3 (148 ± 15%, P < 0.04), monocyte chemoattractant protein-1 (156 ± 16%, P < 0.03), and keratinocyte-derived chemokine (148 ± 18%, P = 0.045) in 3T3-L1 adipocytes and monocyte chemoattractant protein-1 (496 ± 142%, P < 0.02) and complement C3 (152 ± 25%, P < 0.04) in adipose tissue and primary adipocytes, respectively. These SP effects were accompanied by downregulation of insulin receptor substrate 1 (−82 ± 2%, P < 0.01) and GLUT4 (−76 ± 2%, P < 0.01) mRNA expression, and SP acutely blocked insulin-mediated stimulation of fatty acid uptake and Akt phosphorylation. Although adiponectin secretion was unchanged, mRNA expression was decreased (−86 ± 8%, P < 0.001). In humans, NK1R expression correlates positively with plasma insulin, fatty acid, and complement C3 and negatively with adiponectin, CEBPα, CEBPβ, and peroxisome proliferator-activated receptor-γ mRNA expression in omental, but not subcutaneous, adipose tissue. Our results suggest that, beyond its neuroendocrine and inflammatory effects, SP could also be involved in targeting adipose tissue and influencing insulin resistance.

scholarly journals Lipid storage by adipose tissue macrophages regulates systemic glucose tolerance

2014 ◽  
Vol 307 (4) ◽  
pp. E374-E383 ◽  
Author(s):  
Myriam Aouadi ◽  
Pranitha Vangala ◽  
Joseph C. Yawe ◽  
Michaela Tencerova ◽  
Sarah M. Nicoloro ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Fatty Acid Uptake ◽  
Foam Cell Formation ◽  
Acid Uptake ◽  
Obese Mice ◽  
Adipose Tissue Macrophages

Proinflammatory pathways in adipose tissue macrophages (ATMs) can impair glucose tolerance in obesity, but ATMs may also be beneficial as repositories for excess lipid that adipocytes are unable to store. To test this hypothesis, we selectively targeted visceral ATMs in obese mice with siRNA against lipoprotein lipase (LPL), leaving macrophages within other organs unaffected. Selective silencing of ATM LPL decreased foam cell formation in visceral adipose tissue of obese mice, consistent with a reduced supply of fatty acids from VLDL hydrolysis. Unexpectedly, silencing LPL also decreased the expression of genes involved in fatty acid uptake (CD36) and esterification in ATMs. This deficit in fatty acid uptake capacity was associated with increased circulating serum free fatty acids. Importantly, ATM LPL silencing also caused a marked increase in circulating fatty acid-binding protein-4, an adipocyte-derived lipid chaperone previously reported to induce liver insulin resistance and glucose intolerance. Consistent with this concept, obese mice with LPL-depleted ATMs exhibited higher hepatic glucose production from pyruvate and glucose intolerance. Silencing CD36 in ATMs also promoted glucose intolerance. Taken together, the data indicate that LPL secreted by ATMs enhances their ability to sequester excess lipid in obese mice, promoting systemic glucose tolerance.

scholarly journals Basal and cold-induced fatty acid uptake of human brown adipose tissue is impaired in obesity

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
T. J. Saari ◽  
J. Raiko ◽  
M. U-Din ◽  
T. Niemi ◽  
M. Taittonen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Brown Adipose

scholarly journals Ovarian Cycle-Specific Regulation of Adipose Tissue Lipid Storage by Testosterone in Female Nonhuman Primates

Endocrinology ◽  
2013 ◽  
Vol 154 (11) ◽  
pp. 4126-4135 ◽  
Author(s):  
Oleg Varlamov ◽  
Michael P. Chu ◽  
Whitney K. McGee ◽  
Judy L. Cameron ◽  
Robert W. O'Rourke ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Sex Hormones ◽  
Luteal Phase ◽  
Fatty Acid Uptake ◽  
Ovarian Cycle ◽  
Lipid Storage ◽  
Hormone Sensitive Lipase ◽  
Acid Uptake ◽  
Hormone Sensitive

Previous studies in rodents and humans suggest that hyperandrogenemia causes white adipose tissue (WAT) dysfunction in females, although the underlying mechanisms are poorly understood. In light of the differences in the length of the ovarian cycle between humans and rodents, we used a nonhuman primate model to elucidate the effects of chronic hyperandrogenemia on WAT function in vivo. Female rhesus macaques implanted with testosterone capsules developed insulin resistance and altered leptin secretion on a high-fat, Western-style diet. In control visceral WAT, lipolysis and hormone-sensitive lipase expression were upregulated during the luteal phase compared with the early follicular (menses) phase of the ovarian cycle. Hyperandrogenemia attenuated elevated lipolysis and hormone-sensitive lipase activity in visceral WAT during the luteal phase but not during menses. Under control conditions, insulin-stimulated Akt and Erk activation and fatty acid uptake in WAT were not significantly affected by the ovarian cycle. In contrast, testosterone treatment preferentially increased fatty acid uptake and insulin signaling at menses. The fatty acid synthase and glucose transporter-4 genes were upregulated by testosterone during the luteal phase. In summary, this study reveals ovarian stage-specific fluctuations in adipocyte lipolysis and suggests that male sex hormones increase and female sex hormones decrease lipid storage in female WAT.

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