scholarly journals The effect of obesity, impaired carbohydrate metabolism and bariatric surgery on adiponectin and leptin mRNA levels in different adipose tissue depots

2020 ◽  
Vol 25 (5) ◽  
pp. 568-576
Author(s):  
L. B. Vasileva ◽  
M. S. Artemyeva ◽  
Yi. Ma ◽  
K. A. Kondratov ◽  
A. D. Anopova ◽  
...  

Objective. To determine the effect of morbid obesity, impaired carbohydrate metabolism and bariatric surgery on adiponectin and leptin mRNA levels in subcutaneous and visceral adipose tissue.Design and methods. The study included 30 obese female patients. Eleven patients had co-existent impaired carbohydrate metabolism. The control group consisted of 10 healthy non-obese women. In all obese patients, subcutaneous and visceral adipose tissue samples were taken during bariatric surgery. In obese patients 1 year after the intervention and in control individuals subcutaneous adipose tissue samples were collected. The circulating levels of adiponectin and leptin were determined by the enzyme immunoassay. The amount of adiponectin and leptin mRNA in adipose tissue were analyzed by real-time polymerase chain reaction.Results. During the first postoperative year, all patients showed a monotonous decrease in body mass index. After the surgery, the circulating levels of adiponectin and leptin returned to reference values (for healthy population). Compared with the control group, obese patients showed 1,4-times lower adiponectin mRNA level (p < 0,01) in subcutaneous adipose tissue, while leptin mRNA level did not change. In obese patients with impaired carbohydrate metabolism, the adiponectin mRNA level was twice lower in visceral adipose tissue (p < 0,01), compared to patients without impaired carbohydrate metabolism. In obese patients with and without impaired carbohydrate metabolism, mRNA levels of adipokines were more than 2-times lower in visceral adipose tissue compared to subcutaneous adipose tissue (p < 0,05). In subcutaneous adipose tissue, 1 year after bariatric intervention, adiponectin mRNA level decreases by 4,5 times (p < 0,01) in obese patients, and leptin mRNA level decreases by 3,1 times (p < 0,01) in patients with obesity and by 1,5 times (p < 0,05) in patients with obesity and impaired carbohydrate metabolism. Neither adiponectin nor leptin mRNA levels from adipose tissue of different localization showed statistically significant correlation. No correlation was found between the levels of circulating adipokines and their mRNA amount in adipose tissue.Conclusions. Our results indicate that adiponectin and leptin mRNA levels in adipose tissue cells depend on their localization in the body, as well as the presence of obesity and impaired carbohydrate metabolism. We also showed that adiponectin and leptin mRNA levels in adipose tissue change in response to bariatric surgery.

2000 ◽  
Vol 83 (04) ◽  
pp. 545-548 ◽  
Author(s):  
Vanessa Van Harmelen ◽  
Johan Hoffstedt ◽  
Per Lundquist ◽  
Hubert Vidal ◽  
Veronika Stemme ◽  
...  

SummaryHigh plasma plasminogen activator inhibitor-1 (PAI-1) activity is a frequent finding in obesity and adipose tissue has recently been suggested to be a source of circulating PAI-1 in humans. In the present study, differences in adipose tissue gene expression and protein secretion rate of PAI-1 between subcutaneous and visceral adipose tissue was analysed in specimens obtained from 22 obese individuals. The secretion rate of PAI-1 was two-fold higher in subcutaneous adipose tissue than in visceral adipose tissue (292 ± 50 vs 138 ± 24 ng PAI-1/107 cells, P <0.05). In accordance with the secretion data, subcutaneous adipose tissue contained about three-fold higher levels of PAI-1 mRNA than visceral adipose tissue (2.43 ± 0.37 vs 0.81 ± 0.12 attomole PAI-1 mRNA/µg total RNA, P <0.001). PAI-1 secretion from subcutaneous but not from visceral adipose tissue correlated significantly with cell size (r = 0.43, P <0.05). In summary, subcutaneous adipose tissue secreted greater amounts of PAI-1 and had a higher PAI-1 gene expression than visceral adipose tissue from the same obese individuals. Bearing in mind that subcutaneous adipose tissue is the largest fat depot these finding may be important for the coagulation abnormalities associated with obesity.


2019 ◽  
Vol 91 (3) ◽  
pp. 400-410 ◽  
Author(s):  
Judith Brock ◽  
Andreas Schmid ◽  
Thomas Karrasch ◽  
Petra Pfefferle ◽  
Jutta Schlegel ◽  
...  

PLoS ONE ◽  
2017 ◽  
Vol 12 (4) ◽  
pp. e0175133 ◽  
Author(s):  
Inga Schlecht ◽  
Wolfram Gronwald ◽  
Gundula Behrens ◽  
Sebastian E. Baumeister ◽  
Johannes Hertel ◽  
...  

2005 ◽  
Vol 288 (5) ◽  
pp. E930-E934 ◽  
Author(s):  
Neda Rasouli ◽  
Ulrika Raue ◽  
Leslie M. Miles ◽  
Tong Lu ◽  
Gina B. Di Gregorio ◽  
...  

Patients with insulin resistance often manifest increased intramyocellular lipid (IMCL) along with increased visceral adipose tissue. This study was designed to determine whether the insulin sensitizer drugs pioglitazone and metformin would improve glucose intolerance and insulin sensitivity by decreasing IMCL. In this study, 23 generally healthy subjects with impaired glucose tolerance were randomized to receive either pioglitazone 45 mg/day or metformin 2,000 mg/day for 10 wk. Before and after treatment, we measured insulin sensitivity and abdominal subcutaneous and visceral adipose tissue with CT scanning. In addition, muscle biopsies were performed for measurement of IMCL and muscle oxidative enzymes. After treatment with pioglitazone, 2-h glucose fell from 9.6 mmol/l (172 mg/dl) to 6.1 mmol/l (119 mg/dl), whereas there was no change in 2-h glucose with metformin. With pioglitazone treatment, there was a 65% increase in insulin sensitivity along with a 34% decrease in IMCL (both P ≤ 0.002). This decrease in IMCL was not due to increased muscle lipid oxidation, as there were no changes in muscle lipid oxidative enzymes. However, pioglitazone resulted in a 2.6-kg weight gain along with a significant decrease in the visceral-to-subcutaneous adipose tissue ratio. In contrast, metformin treatment resulted in no change in insulin sensitivity, IMCL, oxidative enzymes, or adipose tissue volumes. Pioglitazone improved glucose tolerance and insulin sensitivity by reducing IMCL. This reduction in IMCL was not due to an increase in muscle lipid oxidation but to a diversion of lipid from ectopic sites into subcutaneous adipose tissue.


2007 ◽  
Vol 293 (4) ◽  
pp. E958-E964 ◽  
Author(s):  
Gregory R. Steinberg ◽  
Bruce E. Kemp ◽  
Matthew J. Watt

We have investigated the gene and protein expression of adipose triglyceride lipase (ATGL) and triglyceride (TG) lipase activity from subcutaneous and visceral adipose tissue of lean and obese subjects. Visceral and subcutaneous adipose tissue was obtained from 16 age-matched lean and obese subjects during abdominal surgery. Tissues were analyzed for mRNA expression of lipolytic enzymes by real-time quantitative PCR. ATGL protein content was assessed by Western blot and TG lipase activity by radiometric assessment. Subcutaneous and visceral adipose tissue of obese subjects had elevated mRNA expression of PNPLA2 (ATGL) and other lipases including PNPLA3, PNPLA4, CES1, and LYPLAL1 ( P < 0.05). Surprisingly, ATGL protein expression and TG lipase activity were reduced in subcutaneous adipose tissue of obese subjects. Immunoprecipitation of ATGL reduced total TG lipase activity in adipose lysates by 70% in obese and 83% in lean subjects. No significant differences in the ATGL activator CGI-58 mRNA levels ( ABHD5) were associated with obesity. These data demonstrate that ATGL is important for efficient TG lipase activity in humans. They also demonstrate reduced ATGL protein expression and TG lipase activity despite increased mRNA expression of ATGL and other novel lipolytic enzymes in obesity. The lack of correlation between ATGL protein content and in vitro TG lipase activity indicates that small decrements in ATGL protein expression are not responsible for the reduction in TG lipase activity observed here in obesity, and that posttranslational modifications may be important.


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