scholarly journals Glycerolipid biosynthesis in rat adipose tissue. Influence of adipose-cell size and site of adipose tissue on triacylglycerol formation in lean and obese rats

1978 ◽  
Vol 170 (1) ◽  
pp. 153-160 ◽  
Author(s):  
S C Jamdar
Keyword(s):  
Adipose Tissue ◽  
Lipid Synthesis ◽  
Fat Depots ◽  
Lipid Formation ◽  
Obese Rats ◽  
Fat Depot ◽  
Esterification Reactions ◽  
Rat Adipose Tissue ◽  
Adipose Organ ◽  
Subcutaneous Adipose

The rates of lipid formation were compared in different fat-depots from lean and obese rats by using [14C]glycerol 3-phosphate, [14C]glucose or [14C]acetate as substrates. In lean animals, subcutaneous adipose tissue showed significantly lower rates of lipid synthesis than did perirenal and gonadal fat-tissue. In obese animals, the rates of lipid synthesis were significantly higher and did not vary from one fat-depot to another. Differences in the rates of lipid formation between lean and obese rats disappeared during dietary restriction of obese animals. The isolated adipocyte preparation did not reflect the true metabolic activity of the adipose organ, since this preparation was mainly derived from smaller adipocytes that were metabolically less active than larger adipocytes. The present study suggests that it is better to use whole tissue preparations to measure lipogenesis and esterification reactions, because these measurements represent the contribution of both larger and smaller adipocytes towards lipid formation.

scholarly journals Glycerolipid biosynthesis in rat adipose tissue. Influence of adipocyte size

1981 ◽  
Vol 194 (1) ◽  
pp. 293-298 ◽  
Author(s):  
S C Jamdar ◽  
L J Osborne ◽  
J A Zeigler
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Fat ◽  
Diacylglycerol Acyltransferase ◽  
Adipocyte Size ◽  
Filtration Method ◽  
Fat Depots ◽  
Lipid Formation ◽  
Phosphatidate Phosphohydrolase ◽  
One Step ◽  
Rat Adipose Tissue

A simple one-step filtration method is described to separate larger adipocytes from the smaller ones by using nylon screen (52 microM pore size). Adipocytes retained on the screen were larger (60-90 micrometers) compared with those that passed through the screen. By using this separation technique, activities of various enzymes involved in triacylglycerol formation from sn-glycerol 3-phosphate were measured in the larger and smaller adipocytes isolated from gonadal fat-depots. The homogenates from larger adipocytes were more active in lipid formation compared with those derived from small adipocytes. This was evident from the increased activities of sn-glycerol 3-phosphate acyltransferase. Mg2+-dependent phosphatidate phosphohydrolase and diacylglycerol acyltransferase in the larger adipocytes. The activities of these enzymes were also measured in the adipocytes isolated from gonadal, perirenal and subcutaneous fat-depots. Subcutaneous adipocytes were smaller and were less active in lipid formation than gonadal and perirenal adipocytes. These measurements in the activities of individual enzymes provide evidence that the entire pathway of esterification via sn-glycerol 3-phosphate is accelerated in the larger adipocytes.

scholarly journals Galanin inhibits leptin expression and secretion in rat adipose tissue and 3T3-L1 adipocytes

2004 ◽  
Vol 33 (1) ◽  
pp. 11-19 ◽  
Author(s):  
RY Li ◽  
HD Song ◽  
WJ Shi ◽  
SM Hu ◽  
YS Yang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Mrna Expression ◽  
Vital Role ◽  
Dependent Manner ◽  
Protein Levels ◽  
Orexigenic Peptide ◽  
Fat Depot ◽  
Rat Adipose Tissue ◽  
Leptin Expression

In addition to serving as a fat depot, adipose tissue is also considered as an important endocrine organ that synthesizes and secretes a number of factors. Leptin is an adipocyte-derived hormone that plays a vital role in energy balance. Expression of leptin is regulated by dietary status and hormones. In the present study, we report that galanin, an orexigenic peptide, inhibits leptin expression and secretion in rat adipose tissue and in 3T3-L1 adipocytes. Treatment with galanin (25 micro g/animal) induced approximately 46% down-regulation of leptin secretion at 15 min, followed by 40, 37 and 47% decreases in leptin secretion at 1, 2 and 4 h respectively. Although Northern blot analysis of adipose tissue from the same animals showed that leptin mRNA expression in adipose tissue was unaffected by galanin treatment for 2 h, galanin treatment for 4 h led to decline of leptin mRNA expression in a dose-dependent manner. Meanwhile, treating the rats with galanin had no effect on leptin mRNA expression in the hypothalamus. The inhibitory action of the galanin on leptin mRNA and protein levels was also observed in vitro. When incubated with 10 nM galanin for 48 h, leptin mRNA expression and protein secretion also decreased in 3T3-L1 adipocytes. On the other hand, galanin was found not only to express in rat adipose tissue, but also to increase about 8-fold after fasting. Based on these data, we speculate that increased galanin expression in rat adipose tissue after fasting may be involved in reducing leptin expression and secretion in fasting rats.

scholarly journals Distinct infrastructure of lipid networks in visceral and subcutaneous adipose tissues in overweight humans

2020 ◽  
Vol 112 (4) ◽  
pp. 979-990
Author(s):  
Anish Zacharia ◽  
Daniel Saidemberg ◽  
Chanchal Thomas Mannully ◽  
Natalya M Kogan ◽  
Alaa Shehadeh ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Metabolic Diseases ◽  
Cell Model ◽  
Subcutaneous Tissue ◽  
Embryonic Stem ◽  
Adipose Tissues ◽  
Fat Depots ◽  
Visceral Adipose ◽  
Subcutaneous Adipose

ABSTRACT Background Adipose tissue plays important roles in health and disease. Given the unique association of visceral adipose tissue with obesity-related metabolic diseases, the distribution of lipids between the major fat depots located in subcutaneous and visceral regions may shed new light on adipose tissue–specific roles in systemic metabolic perturbations. Objective We sought to characterize the lipid networks and unveil differences in the metabolic infrastructure of the 2 adipose tissues that may have functional and nutritional implications. Methods Paired visceral and subcutaneous adipose tissue samples were obtained from 17 overweight patients undergoing elective abdominal surgery. Ultra-performance LC-MS was used to measure 18,640 adipose-derived features; 520 were putatively identified. A stem cell model for adipogenesis was used to study the functional implications of the differences found. Results Our analyses resulted in detailed lipid metabolic maps of the 2 major adipose tissues. They point to a higher accumulation of phosphatidylcholines, triacylglycerols, and diacylglycerols, although lower ceramide concentrations, in subcutaneous tissue. The degree of unsaturation was lower in visceral adipose tissue (VAT) phospholipids, indicating lower unsaturated fatty acid incorporation into adipose tissue. The differential abundance of phosphatidylcholines we found can be attributed at least partially to higher expression of phosphatidylethanolamine methyl transferase (PEMT). PEMT-deficient embryonic stem cells showed a dramatic decrease in adipogenesis, and the resulting adipocytes exhibited lower accumulation of lipid droplets, in line with the lower concentrations of glycerolipids in VAT. Ceramides may inhibit the expression of PEMT by increased insulin resistance, thus potentially suggesting a functional pathway that integrates ceramide, PEMT, and glycerolipid biosynthetic pathways. Conclusions Our work unveils differential infrastructure of the lipid networks in visceral and subcutaneous adipose tissues and suggests an integrative pathway, with a discriminative flux between adipose tissues.

scholarly journals Peripancreatic adipose tissue protects against high-fat-diet-induced hepatic steatosis and insulin resistance in mice

2020 ◽  
Vol 44 (11) ◽  
pp. 2323-2334
Author(s):  
Belén Chanclón ◽  
Yanling Wu ◽  
Milica Vujičić ◽  
Marco Bauzá-Thorbrügge ◽  
Elin Banke ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Insulin Levels ◽  
Fat Depots ◽  
Fat Depot

Abstract Background/objectives Visceral adiposity is associated with increased diabetes risk, while expansion of subcutaneous adipose tissue may be protective. However, the visceral compartment contains different fat depots. Peripancreatic adipose tissue (PAT) is an understudied visceral fat depot. Here, we aimed to define PAT functionality in lean and high-fat-diet (HFD)-induced obese mice. Subjects/methods Four adipose tissue depots (inguinal, mesenteric, gonadal, and peripancreatic adipose tissue) from chow- and HFD-fed male mice were compared with respect to adipocyte size (n = 4–5/group), cellular composition (FACS analysis, n = 5–6/group), lipogenesis and lipolysis (n = 3/group), and gene expression (n = 6–10/group). Radioactive tracers were used to compare lipid and glucose metabolism between these four fat depots in vivo (n = 5–11/group). To determine the role of PAT in obesity-associated metabolic disturbances, PAT was surgically removed prior to challenging the mice with HFD. PAT-ectomized mice were compared to sham controls with respect to glucose tolerance, basal and glucose-stimulated insulin levels, hepatic and pancreatic steatosis, and gene expression (n = 8–10/group). Results We found that PAT is a tiny fat depot (~0.2% of the total fat mass) containing relatively small adipocytes and many “non-adipocytes” such as leukocytes and fibroblasts. PAT was distinguished from the other fat depots by increased glucose uptake and increased fatty acid oxidation in both lean and obese mice. Moreover, PAT was the only fat depot where the tissue weight correlated positively with liver weight in obese mice (R = 0.65; p = 0.009). Surgical removal of PAT followed by 16-week HFD feeding was associated with aggravated hepatic steatosis (p = 0.008) and higher basal (p < 0.05) and glucose-stimulated insulin levels (p < 0.01). PAT removal also led to enlarged pancreatic islets and increased pancreatic expression of markers of glucose-stimulated insulin secretion and islet development (p < 0.05). Conclusions PAT is a small metabolically highly active fat depot that plays a previously unrecognized role in the pathogenesis of hepatic steatosis and insulin resistance in advanced obesity.

Acetyl-CoA Regulation, OXPHOS Integrity and Leptin Levels Are Different in Females With Childhood vs Adulthood Onset of Obesity

Endocrinology ◽  
2020 ◽  
Vol 161 (11) ◽  
Author(s):  
Bjorn T Tam ◽  
Jessica Murphy ◽  
Natalie Khor ◽  
Jose A Morais ◽  
Sylvia Santosa
Keyword(s):  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Clinical Manifestations ◽  
Atp Citrate Lyase ◽  
Acetyl Coa ◽  
Metabolic Intermediate ◽  
Fat Depots ◽  
Regional Body Composition ◽  
Subcutaneous Adipose ◽  
H3 Acetylation

Abstract Although childhood-onset obesity (CO) and adulthood-onset obesity (AO) are known to lead to distinctive clinical manifestations and disease risks, the fundamental differences between them are largely unclear. The aim of the current study is to investigate the fundamental differences between subcutaneous adipose tissue from CO and AO and to identify metabolic differences between abdominal (abSAT) and femoral subcutaneous adipose tissues (feSAT). Total and regional body composition was assessed using dual-energy x-ray absorptiometry (DXA) and computed tomography. Levels of acetyl-CoA, NAD+/NADH, acetyl-CoA network genes, mitochondrial complex abundance, H3 acetylation were determined in biopsied abSAT and feSAT. Serum leptin and adiponectin were measured. Our results showed that acetyl-CoA was higher in subcutaneous adipose tissue from subjects with AO compared with CO. Multiple linear regression revealed that ATP citrate lyase was the only main effect affecting the level of acetyl-CoA. Circulating leptin concentrations was higher in AO. The increased level of acetyl-CoA was strongly associated with histone H3 acetylation, LEP expression in adipose tissue, and circulating leptin in AO. NAD+/NADH was higher in CO; however, abundance of mitochondrial complexes, the complex II:complex V ratio, and the complex IV:complex V ratio were lower in CO, reflecting compromised mitochondrial function in subcutaneous adipose tissue from CO. Moreover, we identified differences in the level of acetyl-CoA and NAD+/NADH ratio between abSAT and feSAT, suggesting that these fat depots may possess different metabolic properties. The fundamental difference in the important metabolic intermediate acetyl-CoA between CO and AO may help us better understand the development of obesity and the pathogenesis of different obesity-related diseases in humans.

Microsomal glycerolphosphate acyltransferase inactivation by fatty acids

1990 ◽  
Vol 68 (9) ◽  
pp. 1255-1260 ◽  
Author(s):  
V. Durocher ◽  
M. Miller ◽  
M. A. Rodriguez
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Serum Albumin ◽  
Membrane Lipids ◽  
Lipid Synthesis ◽  
Acyltransferase Activity ◽  
Molar Ratios ◽  
Rat Adipose Tissue

Glycerolphosphate acyltransferase activity in microsomes from rat adipose tissue is shown to decrease with time upon incubation with adipose tissue cytosolic fraction. The inactivation can be prevented with serum albumin and seems to be caused by an increase in endogenous free fatty acid as a consequence of the action of cytosolic lipase(s) on the membrane lipids. Similar inactivation can be observed after short incubation of microsomes with oleic acid at micromolar concentrations. Diacylglycerol acyltransferase is also inhibited by oleic acid, although to a lesser degree. In contrast, glucose-6-phosphatase and NADPH – cytochrome reductase activities are not changed. The oleic acid effect appears to occur upon binding to the microsomal membranes and can be prevented by bovine serum albumin at protein/fatty acid molar ratios above one. These results suggest that free fatty acids may be involved in the modulation of triacylglycerol synthetic enzymes.Key words: glycerolphosphate acyltransferase, fatty acids, microsomal enzymes, lipid synthesis.

scholarly journals Estrogen Controls Lipolysis by Up-Regulating α2A-Adrenergic Receptors Directly in Human Adipose Tissue through the Estrogen Receptor α. Implications for the Female Fat Distribution

2004 ◽  
Vol 89 (4) ◽  
pp. 1869-1878 ◽  
Author(s):  
Steen B. Pedersen ◽  
Kurt Kristensen ◽  
Pernille A. Hermann ◽  
John A. Katzenellenbogen ◽  
Bjørn Richelsen
Keyword(s):  
Estrogen Receptor ◽  
Adipose Tissue ◽  
Adrenergic Receptors ◽  
Human Adipose Tissue ◽  
Fat Distribution ◽  
Receptor Subtype ◽  
Fat Depots ◽  
Fat Depot

Abstract Estrogen seems to promote and maintain the typical female type of fat distribution that is characterized by accumulation of adipose tissue, especially in the sc fat depot, with only modest accumulation of adipose tissue intraabdominally. However, it is completely unknown how estrogen controls the fat accumulation. We studied the effects of estradiol in vivo and in vitro on human adipose tissue metabolism and found that estradiol directly increases the number of antilipolytic α2A-adrenergic receptors in sc adipocytes. The increased number of α2A-adrenergic receptors caused an attenuated lipolytic response of epinephrine in sc adipocytes; in contrast, no effect of estrogen on α2A-adrenergic receptor mRNA expression was observed in adipocytes from the intraabdominal fat depot. These findings show that estrogen lowers the lipolytic response in sc fat depot by increasing the number of antilipolytic α2A-adrenergic receptors, whereas estrogen seems not to affect lipolysis in adipocytes from the intraabdominal fat depot. Using estrogen receptor subtype-specific ligands, we found that this effect of estrogen was caused through the estrogen receptor subtype α. These findings demonstrate that estrogen attenuates the lipolytic response through up-regulation of the number of antilipolytic α2A-adrenergic receptors only in sc and not in visceral fat depots. Thus, our findings offer an explanation how estrogen maintains the typical female sc fat distribution because estrogen seems to inhibit lipolysis only in sc depots and thereby shifts the assimilation of fat from intraabdominal depots to sc depots.

Alterations in rat adipose tissue morphology induced by a low-temperature environment

1982 ◽  
Vol 242 (2) ◽  
pp. E93-E96 ◽  
Author(s):  
W. H. Miller ◽  
I. M. Faust
Keyword(s):  
Adipose Tissue ◽  
Sprague Dawley ◽  
High Fat ◽  
Fat Depots ◽  
High Carbohydrate ◽  
Tissue Morphology ◽  
Age Related ◽  
Sprague Dawley Rats ◽  
Temperature Environment ◽  
Rat Adipose Tissue

Rats raised in the cold showed an unusual pattern of adipose tissue morphology. Male Sprague-Dawley rats were maintained in a 5 degrees C environment for up to 24 wk and the cellularity of their major adipose depots was determined. Normal age-related increases in adipocyte number were absent in two major fat depots (retroperitoneal and inguinal), whereas there was a supranormal increase in a third (epididymal). This pattern of hyperplasia contrasts sharply with that seen in rats fed highly palatable high-fat or high-carbohydrate diets in which retroperitoneal depots show the most hyperplasia and epididymal pads the least. Such variations of response across depots suggest that the features of adipose tissue responsible for adipocyte proliferation in the various depots may not be homogeneous both in their nature and in their distribution.

scholarly journals Transcriptomic profiling of adipose tissue inflammation, remodeling, and lipid metabolism in periparturient dairy cows (Bos taurus)

BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
David Salcedo-Tacuma ◽  
Jair Parales-Giron ◽  
Crystal Prom ◽  
Miguel Chirivi ◽  
Juliana Laguna ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Radical Scavenging ◽  
Lipid Synthesis ◽  
Molecular Transport ◽  
Enrichment Analysis ◽  
Functional Enrichment Analysis ◽  
Functional Enrichment ◽  
Matrix Remodeling ◽  
Adipose Organ

Abstract Background Periparturient cows release fatty acid reserves from adipose tissue (AT) through lipolysis in response to the negative energy balance induced by physiological changes related to parturition and the onset of lactation. However, lipolysis causes inflammation and structural remodeling in AT that in excess predisposes cows to disease. The objective of this study was to determine the effects of the periparturient period on the transcriptomic profile of AT using NGS RNAseq. Results Subcutaneous AT samples were collected from Holstein cows (n = 12) at 11 ± 3.6 d before calving date (PreP) and at 6 ± 1d (PP1) and 13 ± 1.4d (PP2) after parturition. Differential expression analyses showed 1946 and 1524 DEG at PP1 and PP2, respectively, compared to PreP. Functional Enrichment Analysis revealed functions grouped in categories such as lipid metabolism, molecular transport, energy production, inflammation, and free radical scavenging to be affected by parturition and the onset of lactation (FDR < 0.05). Inflammation related genes such as TLR4 and IL6 were categorized as upstream lipolysis triggers. In contrast, FASN, ELOVL6, ACLS1, and THRSP were identified as upstream inhibitors of lipid synthesis. Complement (C3), CXCL2, and HMOX1 were defined as links between inflammatory pathways and those involved in the generation of reactive oxygen species. Conclusions Results offer a comprehensive characterization of gene expression dynamics in periparturient AT, identify upstream regulators of AT function, and demonstrate complex interactions between lipid mobilization, inflammation, extracellular matrix remodeling, and redox signaling in the adipose organ.

Effect of phenoxybenzamine on development of adipose tissue in lean and obese Zucker rats

1982 ◽  
Vol 243 (5) ◽  
pp. E398-E406
Author(s):  
K. Comai ◽  
A. C. Sullivan
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Cell Size ◽  
Body Weight Gain ◽  
Zucker Rats ◽  
Fat Cell ◽  
Fat Depots ◽  
Fat Cell Size ◽  
Obese Rats ◽  
Fat Depot

Young male Zucker lean (Fa/-) and obese (fa/fa) rats were fed the alpha-adrenergic blocking agent phenoxybenzamine as a dietary admixture for 35 days. In lean and obese rats, phenoxybenzamine treatment decreased significantly body weight gain, food consumption, grams of carcass fat, and grams of carcass protein. Lean rats exhibited reduced fat cell size and number in retroperitoneal, epididymal, and inguinal fat depots. Obese rats treated with phenoxybenzamine exhibited significantly decreased numbers of fat cells in the retroperitoneal, epididymal, and inguinal fat depots and a small decreased cell size in the inguinal fat depot only. The levels of carcass fat and protein and fat cell number in obese and lean rats treated with phenoxybenzamine for 35 days were similar to pretreatment values in agreement with the lack of body weight gain. Although values in agreement with the lack of body weight gain. Although rats exhibited marked decreases in fat accumulation during phenoxybenzamine treatment, fat cell size and number returned to control values during the posttreatment period with a marked hyperplasia occurring particularly in the retroperitoneal fat depot of obese rats. Serum levels of insulin were suppressed and free fatty acid levels increased in obese rats during phenoxybenzamine treatment, suggesting a stimulation of the sympathoadrenal system. This study shows that despite severe restrictions in fat cell proliferation during the rapid-growth phase of the obese Zucker rat, the mechanisms for cellular proliferation and fat deposition remain intact.

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