scholarly journals Apolipoprotein A-IV Enhances Fatty Acid Uptake by Adipose Tissues of Male Mice via Sympathetic Activation

Endocrinology ◽  
2020 ◽  
Vol 161 (4) ◽  
Author(s):  
Qi Zhu ◽  
Jonathan Weng ◽  
Minqian Shen ◽  
Jace Fish ◽  
Zhujun Shen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Sympathetic Activity ◽  
Sympathetic Innervation ◽  
Acid Uptake ◽  
Adipose Tissues ◽  
Lipid Mixture ◽  
Apolipoprotein A ◽  
Brown Adipose

Abstract Apolipoprotein A-IV (ApoA-IV) synthesized by the gut regulates lipid metabolism. Sympathetic innervation of adipose tissues also controls lipid metabolism. We hypothesized that ApoA-IV required sympathetic innervation to increase fatty acid (FA) uptake by adipose tissues and brown adipose tissue (BAT) thermogenesis. After 3 weeks feeding of either a standard chow diet or a high-fat diet (HFD), mice with unilateral denervation of adipose tissues received intraperitoneal administration of recombinant ApoA-IV protein and intravenous infusion of lipid mixture with radioactive triolein. In chow-fed mice, ApoA-IV administration increased FA uptake by intact BAT but not the contralateral denervated BAT or intact white adipose tissue (WAT). Immunoblots showed that, in chow-fed mice, ApoA-IV increased expression of lipoprotein lipase and tyrosine hydroxylase in both intact BAT and inguinal WAT (IWAT), while ApoA-IV enhanced protein levels of β3 adrenergic receptor, adipose triglyceride lipase, and uncoupling protein 1 in the intact BAT only. In HFD-fed mice, ApoA-IV elevated FA uptake by intact epididymal WAT (EWAT) but not intact BAT or IWAT. ApoA-IV increased sympathetic activity assessed by norepinephrine turnover (NETO) rate in BAT and EWAT of chow-fed mice, whereas it elevated NETO only in EWAT of HFD-fed mice. These observations suggest that, in chow-fed mice, ApoA-IV activates sympathetic activity of BAT and increases FA uptake by BAT via innervation, while in HFD-fed mice, ApoA-IV stimulates sympathetic activity of EWAT to shunt FAs into the EWAT.

Fatty acid synthesis in adipose tissues of physically trained rats in vivo

1983 ◽  
Vol 245 (1) ◽  
pp. E8-E13
Author(s):  
K. Tokuyama ◽  
H. Okuda
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Physical Training ◽  
Dark Period ◽  
Acid Synthesis ◽  
Free Access ◽  
Adipose Tissues ◽  
Brown Adipose

The effect of physical training on fatty acid synthesis in vivo was studied. After the rats had free access to a running wheel for 50 days, the rate of fatty acid synthesis estimated using 3H2O in adipose tissues of trained rats was about three times higher than that of sedentary rats in both the light and dark period. The rate of fatty acid synthesis in the liver but not in the brown adipose tissue was also slightly enhanced by physical training. The number of adipocytes was not affected, but the size of adipocytes was reduced by physical training. In trained rats, the rate of fatty acid synthesis in adipocytes whose diameter was similar to that of sedentary rats was about 10 times higher than that of sedentary rats. Within adipose tissue, the rate of fatty acid synthesis correlated positively to the diameter of adipocytes both in the sedentary and trained rats. These findings mean that the adaptive increase in fatty acid synthesis seen in adipocytes of trained rats is not secondary to the reduction in size of adipocytes.

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 Lipid metabolism in women

2004 ◽  
Vol 63 (1) ◽  
pp. 153-160 ◽  
Author(s):  
Christine M. Williams
Keyword(s):  
Adipose Tissue ◽  
Cardiovascular Risk ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Body Fat ◽  
Adrenergic Receptors ◽  
Subcutaneous Fat ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Fat Depots

Differences in whole-body lipid metabolism between men and women are indicated by lower-body fat accumulation in women but more marked accumulation of fat in the intra-abdominal visceral fat depots of men. Circulating blood lipid concentrations also show gender-related differences. These differences are most marked in premenopausal women, in whom total cholesterol, LDL-cholesterol and triacylglycerol concentrations are lower and HDL-cholesterol concentration is higher than in men. Tendency to accumulate body fat in intra-abdominal fat stores is linked to increased risk of CVD, metabolic syndrome, diabetes and other insulin-resistant states. Differential regional regulation of adipose tissue lipolysis and lipogenesis must underlie gender-related differences in the tendency to accumulate fat in specific fat depots. However, empirical data to support current hypotheses remain limited at the present time because of the demanding and specialist nature of the methods used to study adipose tissue metabolism in human subjects. In vitro and in vivo data show greater lipolytic sensitivity of abdominal subcutaneous fat and lesser lipolytic sensitivity of femoral and gluteal subcutaneous fat in women than in men. These differences appear to be due to fewer inhibitory α adrenergic receptors in abdominal regions and greater α adrenergic receptors in gluteal and femoral regions in women than in men. There do not appear to be major gender-related differences in rates of fatty acid uptake (lipogenesis) in different subcutaneous adipose tissue regions. In visceral fat rates of both lipolysis and lipogenesis appear to be greater in men than in women; higher rates of lipolysis may be due to fewer α adrenergic receptors in this fat depot in men. Fatty acid uptake into this depot in the postprandial period is approximately 7-fold higher in men than in women. Triacylglycerol concentrations appear to be a stronger cardiovascular risk factor in women than in men, with particular implications for cardiovascular risk in diabetic women. The increased triacylglycerol concentrations observed in women taking hormone-replacement therapy (HRT) may explain the paradoxical findings of increased rates of CVD in women taking HRT that have been reported from recent primary and secondary prevention trials of HRT.

scholarly journals Flattened circadian glucocorticoid oscillations cause obesity due to increased lipid turnover and lipid uptake

2020 ◽  
Author(s):  
Stefan Tholen ◽  
Kyle M. Kovary ◽  
Atefeh Rabiee ◽  
Ewa Bielczyk-Maczyńska ◽  
Wenting Yang ◽  
...  
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Weight Gain ◽  
Lipid Accumulation ◽  
Body Weight Gain ◽  
List Type ◽  
Acid Uptake ◽  
Adipose Tissues ◽  
Brown Adipose ◽  
White Fat

ABSTRACTChronic stressors flatten circadian glucocorticoid (GC) oscillations, which has been correlated with negative health outcomes including obesity. How such flattened circadian GC oscillations affect metabolism and fat storage remains unknown. Here we investigated the consequences in mice and found that flattening of GC oscillations results not only in body weight gain, mainly due to increases in white fat depot mass, but also leads to hyperinsulinemia and fat accumulation in brown adipose tissue. A transcriptomic analysis of white and brown adipose tissues revealed that flattened GC oscillations cause dysregulated lipid metabolism with a prominent role of the fatty acid transporter Cd36. Indeed, Cd36 knockout mice are partially protected against the adverse effects of flattened GC oscillations including body weight gain and lipid accumulation in the brown and visceral white fat depots. These results provide insights on how conditions associated with flattened GC levels cause obesity.HIGHLIGHTSFlattening of circadian GC oscillations in mice, despite keeping mean circulating GC levels the same, results in body weight gain, lipid accumulation in both brown and white adipose tissues (BAT and WAT), and hyperinsulinemia.Markedly, flattening GC oscillations for short periods of three days is sufficient to increase lipid accumulation and mass in BAT, but longer periods are needed to increase lipid accumulation and mass in WAT.Transcriptomics analysis shows increased expression of a key regulator of fatty acid uptake, CD36, and knockout of CD36 partially protects cells from flattening GC oscillations

Effect of the β-adrenoceptor agonist BRL 26830 on fatty acid synthesis and on the activities of pyruvate dehydrogenase and acetyl-CoA carboxylase in adipose tissues of the rat

1989 ◽  
Vol 9 (1) ◽  
pp. 111-117 ◽  
Author(s):  
Shelagh Wilson
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Brown Adipose Tissue ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Diabetic Rats ◽  
Adipose Tissues ◽  
Adrenoceptor Agonist ◽  
Brown Adipose

BRL 26830 is a thermogenic β-adrenoceptor agonist which stimulates lipolysis and fatty acid oxidation in vivo. It also stimulates insulin secretion, and hence promotes glucose utilisation in vivo. The effect of this agent on white and brown adipose tissue of the rat was investigated. BRL 26830 increased the rate of fatty acid synthesis in vivo in white adipose tissue by 135% but reduced the rate of fatty acid synthesis in vivo in brown adipose tissue by 78%. The increase was abolished in white adipose tissue of streptozotocin-diabetic rats, indicating that the effect involved a rise in circulating insulin levels. The reduction in fatty acid synthesis in brown adipose tissues was associated with a reduction in the activity of acetyl-CoA carboxylase in the tissue consistent with a direct β-adrenoceptor-mediated effect. BRL 26830 also increased the proportion of pyruvate dehydrogenase in its active form in vivo in brown adipose tissue and this increase was abolished in streptozotocin-diabetic rats. These findings illustrate different sensitivities of white and brown adipose tissues to combined β-adrenergic and insulin stimulation.

scholarly journals Metabolic activity of brown, “beige,” and white adipose tissues in response to chronic adrenergic stimulation in male mice

2016 ◽  
Vol 311 (1) ◽  
pp. E260-E268 ◽  
Author(s):  
Sébastien M. Labbé ◽  
Alexandre Caron ◽  
Kanta Chechi ◽  
Mathieu Laplante ◽  
Roger Lecomte ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Metabolic Activity ◽  
Oxidative Activity ◽  
Acid Uptake ◽  
Adrenergic Stimulation ◽  
Brown Adipocytes ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
Beige Adipocytes

Classical brown adipocytes such as those found in interscapular brown adipose tissue (iBAT) represent energy-burning cells, which have been postulated to play a pivotal role in energy metabolism. Brown adipocytes can also be found in white adipose tissue (WAT) depots [e.g., inguinal WAT (iWAT)] following adrenergic stimulation, and they have been referred to as “beige” adipocytes. Whether the presence of these adipocytes, which gives iWAT a beige appearance, can confer a white depot with some thermogenic activity remains to be seen. In consequence, we designed the present study to investigate the metabolic activity of iBAT, iWAT, and epididymal white depots in mice. Mice were either 1) kept at thermoneutrality (30°C), 2) kept at 30°C and treated daily for 14 days with an adrenergic agonist [CL-316,243 (CL)], or 3) housed at 10°C for 14 days. Metabolic activity was assessed using positron emission tomography imaging with fluoro-[18F]deoxyglucose (glucose uptake), fluoro-[18F]thiaheptadecanoic acid (fatty acid uptake), and [11C]acetate (oxidative activity). In each group, substrate uptakes and oxidative activity were measured in anesthetized mice in response to acute CL. Our results revealed iBAT as a major site of metabolic activity, which exhibited enhanced glucose and nonesterified fatty acid uptakes and oxidative activity in response to chronic cold and CL. On the other hand, beige adipose tissue failed to exhibit appreciable increase in oxidative activity in response to chronic cold and CL. Altogether, our results suggest that the contribution of beige fat to acute-CL-induced metabolic activity is low compared with that of iBAT, even after sustained adrenergic stimulation.

scholarly journals Dim Light at Night Disturbs Molecular Pathways of Lipid Metabolism

2020 ◽  
Vol 21 (18) ◽  
pp. 6919
Author(s):  
Monika Okuliarova ◽  
Valentina Sophia Rumanova ◽  
Katarina Stebelova ◽  
Michal Zeman
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Metabolic Diseases ◽  
De Novo ◽  
Negative Impact ◽  
Acid Uptake ◽  
Control Mechanisms ◽  
Light At Night ◽  
Dim Light

Dim light at night (dLAN) is associated with metabolic risk but the specific effects on lipid metabolism have only been evaluated to a limited extent. Therefore, to explore whether dLAN can compromise lipid metabolic homeostasis in healthy individuals, we exposed Wistar rats to dLAN (~2 lx) for 2 and 5 weeks and analyzed the main lipogenic pathways in the liver and epididymal fat pad, including the control mechanisms at the hormonal and molecular level. We found that dLAN promoted hepatic triacylglycerol accumulation, upregulated hepatic genes involved in de novo synthesis of fatty acids, and elevated glucose and fatty acid uptake. These observations were paralleled with suppressed fatty acid synthesis in the adipose tissue and altered plasma adipokine levels, indicating disturbed adipocyte metabolic function with a potential negative impact on liver metabolism. Moreover, dLAN-exposed rats displayed an elevated expression of two peroxisome proliferator-activated receptor family members (Pparα and Pparγ) in the liver and adipose tissue, suggesting the deregulation of important metabolic transcription factors. Together, our results demonstrate that an impaired balance of lipid biosynthetic pathways caused by dLAN can increase lipid storage in the liver, thereby accounting for a potential linking mechanism between dLAN and metabolic diseases.

scholarly journals Upregulation of lipid metabolism genes in the breast prior to cancer diagnosis

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Natascia Marino ◽  
Rana German ◽  
Xi Rao ◽  
Ed Simpson ◽  
Sheng Liu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Normal Tissue ◽  
Fatty Acid Transport ◽  
Acid Uptake ◽  
Healthy Controls ◽  
Breast Epithelium ◽  
Cancer Initiation ◽  
Tissue Compartments

Abstract Histologically normal tissue adjacent to the tumor can provide insight of the microenvironmental alterations surrounding the cancerous lesion and affecting the progression of the disease. However, little is known about the molecular changes governing cancer initiation in cancer-free breast tissue. Here, we employed laser microdissection and whole-transcriptome profiling of the breast epithelium prior to and post tumor diagnosis to identify the earliest alterations in breast carcinogenesis. Furthermore, a comprehensive analysis of the three tissue compartments (microdissected epithelium, stroma, and adipose tissue) was performed on the breast donated by either healthy subjects or women prior to the clinical manifestation of cancer (labeled “susceptible normal tissue”). Although both susceptible and healthy breast tissues appeared histologically normal, the susceptible breast epithelium displayed a significant upregulation of genes involved in fatty acid uptake/transport (CD36 and AQP7), lipolysis (LIPE), and lipid peroxidation (AKR1C1). Upregulation of lipid metabolism- and fatty acid transport-related genes was observed also in the microdissected susceptible stromal and adipose tissue compartments, respectively, when compared with the matched healthy controls. Moreover, inter-compartmental co-expression analysis showed increased epithelium-adipose tissue crosstalk in the susceptible breasts as compared with healthy controls. Interestingly, reductions in natural killer (NK)-related gene signature and CD45+/CD20+ cell staining were also observed in the stromal compartment of susceptible breasts. Our study yields new insights into the cancer initiation process in the breast. The data suggest that in the early phase of cancer development, metabolic activation of the breast, together with increased epithelium-adipose tissue crosstalk may create a favorable environment for final cell transformation, proliferation, and survival.

P53 regulates the lipid metabolism response to metabolic stress in brown adipose tissue

2020 ◽  
Author(s):  
G Lenihan-Geels ◽  
F Garcia-Carrizo ◽  
C Li ◽  
M Oster ◽  
A Prokesch ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Brown Adipose Tissue ◽  
Metabolic Stress ◽  
Brown Adipose
Sign in / Sign up

Export Citation Format

Share Document