scholarly journals Human Adipose Tissue Cannabinoid Receptor 1 Gene Expression Is Not Related to Fat Cell Function or Adiponectin Level

2007 ◽  
Vol 92 (4) ◽  
pp. 1555-1559 ◽  
Author(s):  
Patrik Löfgren ◽  
Eva Sjölin ◽  
Kerstin Wåhlen ◽  
Johan Hoffstedt
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Cell Function ◽  
Cannabinoid Receptor ◽  
Human Adipose Tissue ◽  
Mrna Levels ◽  
Fat Cell ◽  
Cannabinoid Receptor 1 ◽  
Omental Fat ◽  
Cnr1 Gene

Abstract Context: The cannabinoid receptor 1 gene (CNR1) is implicated in adipocyte function. Objective: We investigated human adipose tissue CNR1 mRNA in relation to obesity, clinical and metabolic variables, adipocyte function, and adiponectin (ADIPOQ) levels. Methods: We assessed sc fat biopsies from 96 obese and nonobese subjects and omental fat biopsies from 82 obese and nonobese subjects. Results: The sc and omental adipose CNR1 gene expression were similar in obese and nonobese subjects. No association between either sc or omental adipose CNR1 mRNA levels and body mass index, waist circumference, plasma levels of glucose and insulin, lipids, or blood pressure was found. The sc and omental maximal adrenergic lipolytic activation as well as lipolytic adrenoceptor sensitivity were not related to CNR1 gene expression. Lipogenesis in sc adipocytes also showed no association with CNR1 mRNA levels. Finally, no relation was found between adipose CNR1 gene expression and ADIPOQ mRNA, adipose tissue adiponectin secretion, or circulating adiponectin. Conclusion: We found no association of human adipose tissue CNR1 mRNA expression with measures of body fat, metabolic parameters, fat cell function, or ADIPOQ expression. These data do not suggest a major role of human adipose CNR1 in fat cell function or metabolic disease development.

Acute and chronic regulation of leptin synthesis, storage, and secretion by insulin and dexamethasone in human adipose tissue

2007 ◽  
Vol 292 (3) ◽  
pp. E858-E864 ◽  
Author(s):  
Mi-Jeong Lee ◽  
Yanxin Wang ◽  
Matthew R. Ricci ◽  
Sean Sullivan ◽  
Colleen D. Russell ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Acute Treatment ◽  
Human Adipose Tissue ◽  
Metabolic Labeling ◽  
Mrna Levels ◽  
Fat Cell ◽  
Short Term ◽  
Chronic Effects ◽  
Wide Range ◽  
Highly Correlated

Serum leptin levels are upregulated in proportion to body fat and also increase over the short term in response to meals or insulin. To understand the mechanisms involved, we assessed leptin synthesis and secretion in samples of adipose tissue from subjects with a wide range of BMI. Tissue leptin content and relative rates of leptin biosynthesis, as determined by metabolic labeling, were highly correlated with each other and with BMI and fat cell size. To understand mechanisms regulating leptin synthesis in obesity, we used biosynthetic labeling to directly assess the effects of insulin and glucocorticoids (dexamethasone) on leptin synthesis and secretion in human adipose tissue. Chronic treatment (1–2 days in organ culture) with insulin increased relative rates of leptin biosynthesis without affecting leptin mRNA levels. In contrast, dexamethasone increased leptin mRNA and biosynthesis in parallel. Acute treatment with insulin or dexamethasone (added during 1-h preincubation and 45-min pulse labeling) did not affect relative rates of leptin biosynthesis, but pulse-chase studies showed that addition of insulin nearly doubled the release of [35S]leptin after a 1-h chase. We conclude that the higher leptin stores in adipose tissue of obese humans are maintained by chronic effects of insulin and glucocorticoids acting at pre- and posttranslational levels and that the ability of insulin to increase the release of preformed leptin may contribute to short-term variations in circulating leptin levels.

scholarly journals Role of cannabinoid receptor 1 in human adipose tissue for lipolysis regulation and insulin resistance

Endocrine ◽  
2016 ◽  
Vol 55 (3) ◽  
pp. 839-852 ◽  
Author(s):  
Cherno O. Sidibeh ◽  
Maria J. Pereira ◽  
Joey Lau Börjesson ◽  
Prasad G. Kamble ◽  
Stanko Skrtic ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Cannabinoid Receptor ◽  
Human Adipose Tissue ◽  
Cannabinoid Receptor 1

Deleted in breast cancer 1 plays a functional role in adipocyte differentiation

2015 ◽  
Vol 308 (7) ◽  
pp. E554-E561 ◽  
Author(s):  
José María Moreno-Navarrete ◽  
María Moreno ◽  
Marta Vidal ◽  
Francisco Ortega ◽  
Marta Serrano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Adipocyte Differentiation ◽  
Wide Spectrum ◽  
Human Adipose Tissue ◽  
Mrna Levels ◽  
Negatively Associated ◽  
Adipoq Gene ◽  
Protein Levels

Genetic deletion of Dbc1 in mice reduced adipose tissue senescence and inflammation while promoting an expansion of this tissue. Here, we aimed to investigate DBC1 mRNA and protein levels in human adipose tissue from subjects with a wide spectrum of fat mass ( cohort 1; n = 105) and insulin resistance ( cohort 2; n = 47); we also investigated the effects of DBC1 knockdown on 3T3-L1 adipocyte differentiation. DBC1 mRNA was relatively abundant in both visceral (VAT) and subcutaneous adipose tissue (SAT) (mainly in the adipocyte fraction), being decreased in adipose tissue from obese compared with lean subjects. In both VAT and SAT, DBC1 mRNA levels were negatively associated with BMI and positively associated with age and the expression of PPARγ, GLUT4, IRS1, lipogenic ( FASN, ACACA), lipid droplet-associated genes ( PLIN1, FSP27, ADRP, and TIP47), and lipolytic ( ABDH5, AKAP, and PRKACA) genes but negatively associated with ADIPOQ in VAT. DBC1 mRNA and protein levels were increased in the early stages of adipocyte differentiation of human and 3T3-L1 adipocytes. Dbc1 knockdown (KD) with lentivirus led to enhanced adipocyte differentiation, increasing intracellular lipid accumulation and adipogenic gene expression. In conclusion, although DBC1 gene expression was reduced in adipose tissue from obese subjects, it was negatively associated with ADIPOQ gene expression in VAT, suggesting that DBC1 might promote visceral adipose tissue dysfunction. In vitro data supported the antiadipogenic effects of DBC1.

Metallothionein gene expression and secretion in white adipose tissue

2000 ◽  
Vol 279 (6) ◽  
pp. R2329-R2335 ◽  
Author(s):  
Paul Trayhurn ◽  
Jacqueline S. Duncan ◽  
Anne M. Wood ◽  
John H. Beattie
Keyword(s):  
Gene Expression ◽  
Molecular Weight ◽  
Adipose Tissue ◽  
White Adipose Tissue ◽  
Stromal Vascular Fraction ◽  
Low Molecular Weight ◽  
Secretory Product ◽  
Mrna Levels ◽  
Gene Encoding ◽  
Adrenoceptor Agonist

White adipose tissue (WAT) has been examined to determine whether the gene encoding metallothionein (MT), a low-molecular-weight stress response protein, is expressed in the tissue and whether MT may be a secretory product of adipocytes. The MT-1 gene was expressed in epididymal WAT, with MT-1 mRNA levels being similar in lean and obese ( ob/ ob) mice. MT-1 mRNA was found in each of the main adipose tissue sites (epididymal, perirenal, omental, subcutaneous), and there was no major difference between depots. Separation of adipocytes from the stromal-vascular fraction of WAT indicated that the MT gene (MT-1 and MT-2) was expressed in adipocytes themselves. Treatment of mice with zinc had no effect on MT-1 mRNA levels in WAT, despite strong induction of MT-1 expression in the liver. MT-1 gene expression in WAT was also unaltered by fasting or norepinephrine. However, administration of a β3-adrenoceptor agonist, BRL-35153A, led to a significant increase in MT-1 mRNA. On differentiation of fibroblastic preadipocytes to adipocytes in primary culture, MT was detected in the medium, suggesting that the protein may be secreted from WAT. It is concluded that WAT may be a significant site of MT production; within adipocytes, MT could play an antioxidant role in protecting fatty acids from damage.

scholarly journals In Vitro and in Vivo Calcitonin I Gene Expression in Parenchymal Cells: A Novel Product of Human Adipose Tissue

Endocrinology ◽  
2003 ◽  
Vol 144 (12) ◽  
pp. 5578-5584 ◽  
Author(s):  
Philippe Linscheid ◽  
Dalma Seboek ◽  
Eric S. Nylen ◽  
Igor Langer ◽  
Mirjam Schlatter ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Human Adipose Tissue ◽  
Parenchymal Cells ◽  
I Gene

Influence of age, fat cell weight, and obesity on O2 consumption of human adipose tissue

1989 ◽  
Vol 256 (4) ◽  
pp. E467-E474 ◽  
Author(s):  
P. Hallgren ◽  
L. Sjostrom ◽  
H. Hedlund ◽  
L. Lundell ◽  
L. Olbe
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Energy Expenditure ◽  
Human Adipose Tissue ◽  
Fat Cell ◽  
Cell Weight ◽  
Total Body ◽  
Obese Human ◽  
Open Question ◽  
Partial Weight

The oxygen consumption of human adipose tissue (AT) was determined in 53 adults, lean and obese, and in nine lean boys. The oxygen consumption was positively related to fat cell weight and negatively to age and degree of obesity. Men and women did not differ with respect to oxygen consumption of AT. The positive relationship between oxygen consumption per cell and fat cell size was also demonstrated in size-separated cells from the same donors. Expressed per cell the oxygen consumption was higher in fat cells from obese than in cells from lean subjects, but expressed per gram of tissue the opposite result was found. The oxygen consumption of the total AT organ was higher in obese than in lean subjects. The energy expenditure of AT constituted approximately 4% of the estimated 24-h energy expenditure in both groups. It is concluded that obese subjects do not maintain their obesity because of a reduced energy expenditure of the total AT (or of the total body). After a partial weight reduction in five subjects, the energy metabolism tended to change in direction toward the conditions seen in lean subjects. However, it is still an open question whether the observed energy metabolic aberrations of obese human AT are only secondary to the obese state or partly primary and thus of etiological importance.

scholarly journals Cultured Human Adipose Tissue Pericytes and Mesenchymal Stromal Cells Display a Very Similar Gene Expression Profile

2015 ◽  
Vol 24 (23) ◽  
pp. 2822-2840 ◽  
Author(s):  
Lindolfo da Silva Meirelles ◽  
Tathiane Maistro Malta ◽  
Virgínia Mara de Deus Wagatsuma ◽  
Patrícia Viana Bonini Palma ◽  
Amélia Goes Araújo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Gene Expression Profile ◽  
Mesenchymal Stromal Cells ◽  
Expression Profile ◽  
Stromal Cells ◽  
Human Adipose Tissue ◽  
Similar Gene Expression Profile ◽  
Similar Gene

scholarly journals Genetic ablation of adipocyte PD-L1 reduces tumor growth but accentuates obesity-associated inflammation

2020 ◽  
Vol 8 (2) ◽  
pp. e000964 ◽  
Author(s):  
Bogang Wu ◽  
Huai-Chin Chiang ◽  
Xiujie Sun ◽  
Bin Yuan ◽  
Payal Mitra ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Tumor Growth ◽  
Body Weight Gain ◽  
High Body Mass Index ◽  
Human Adipose Tissue ◽  
Mrna Levels ◽  
Metabolic Dysfunction ◽  
Genetic Ablation ◽  
Tumor Immunosuppression

The programmed death-ligand 1 (PD-L1)-dependent immune checkpoint attenuates host immunity and maintains self-tolerance. Imbalance between protective immunity and immunopathology due to altered PD-L1 signaling can lead to autoimmunity or tumor immunosuppression. The role of the PD-L1-dependent checkpoint in non-immune system is less reported. We previously found that white adipocytes highly express PD-L1. Here we show that adipocyte-specific PD-L1 knockout mice exhibit enhanced host anti-tumor immunity against mammary tumors and melanoma with low or no tumor PD-L1. However, adipocyte PD-L1 ablation in tumor-free mice also exacerbates diet-induced body weight gain, pro-inflammatory macrophage infiltration into adipose tissue, and insulin resistance. Low PD-L1 mRNA levels in human adipose tissue correlate with high body mass index and presence of type 2 diabetes. Therefore, our mouse genetic approach unequivocally demonstrates a cell-autonomous function of adipocyte PD-L1 in promoting tumor growth and inhibiting antitumor immunity. In addition, our work uncovers a previously unrecognized role of adipocyte PD-L1 in mitigating obesity-related inflammation and metabolic dysfunction.

Effect of hypothyroidism on adenylyl cyclase activity and subtype gene expression in brown adipose tissue

1997 ◽  
Vol 273 (2) ◽  
pp. R762-R767 ◽  
Author(s):  
A. Chaudhry ◽  
J. G. Granneman
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Adenylyl Cyclase ◽  
Regulation Of Gene Expression ◽  
Mrna Levels ◽  
Adrenergic Stimulation ◽  
Functional Responses ◽  
Synergistic Interactions ◽  
Brown Adipose

Brown adipose tissue (BAT) expresses several adenylyl cyclase (AC) subtypes, and adrenergic stimulation selectively upregulates AC-III gene expression. Previous studies have described synergistic interactions between the sympathetic nervous system (SNS) and 3,5,3'-triiodothyronine (T3) on the regulation of gene expression in BAT. Because adrenergic stimulation also increases the activity of BAT type II thyroxine 5'-deiodinase (DII) and local T3 generation is important for many functional responses in BAT, we examined the effects of thyroid hormone status on the expression of various AC subtypes. Hypothyroidism selectively increased AC-III mRNA levels in BAT but not in white adipose tissue. Of the other subtypes examined, hypothyroidism did not alter AC-VI mRNA levels and slightly reduced AC-IX mRNA levels in BAT. The increase in AC-III expression was paralleled by an increase in forskolin-stimulated AC activity in BAT membranes. Sympathetic denervation of BAT abolished the increase in both AC activity and AC-III mRNA expression produced by hypothyroidism, but did not affect the expression of other subtypes. Surgical denervation also prevented the induction of AC-III in the cold-stressed euthyroid rat, but injections of T3 failed to alter AC-III expression in intact or denervated BAT. Our results indicate that T3 does not directly affect expression of AC-III. Rather, hypothyroidism increases BAT AC-III expression indirectly via an increase in sympathetic stimulation. Furthermore, our results strongly indicate that the increase in AC activity in hypothyroid BAT is due to increased expression of AC-III.

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