scholarly journals The Possible Role of mRNA Expression Changes of GH/IGF-1/Insulin Axis Components in Subcutaneous Adipose Tissue in Metabolic Disturbances of Patients With Acromegaly

2016 ◽  
pp. 493-503 ◽  
Author(s):  
V. TOUSKOVA ◽  
J. KLOUCKOVA ◽  
V. DUROVCOVA ◽  
Z. LACINOVA ◽  
P. KAVALKOVA ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
Body Fat ◽  
Subcutaneous Adipose Tissue ◽  
Whole Body ◽  
Control Group ◽  
Model Assessment ◽  
Subcutaneous Adipose ◽  
Igfbp 3

We explored the effect of chronically elevated circulating levels of growth hormone (GH)/insulin-like-growth-factor-1 (IGF-1) on mRNA expression of GH/IGF-1/insulin axis components and p85alpha subunit of phosphoinositide-3-kinase (p85alpha) in subcutaneous adipose tissue (SCAT) of patients with active acromegaly and compared these findings with healthy control subjects in order to find its possible relationships with insulin resistance and body composition changes. Acromegaly group had significantly decreased percentage of truncal and whole body fat and increased homeostasis model assessment-insulin resistance (HOMA-IR). In SCAT, patients with acromegaly had significantly increased IGF-1 and IGF-binding protein-3 (IGFBP-3) expression that both positively correlated with serum GH. P85alpha expression in SCAT did not differ from control group. IGF-1 and IGFBP-3 expression in SCAT were not independently associated with percentage of truncal and whole body fat or with HOMA-IR while IGFBP-3 expression in SCAT was an independent predictor of insulin receptor as well as of p85alpha expression in SCAT. Our data suggest that GH overproduction in acromegaly group increases IGF-1 and IGFBP-3 expression in SCAT while it does not affect SCAT p85alpha expression. Increased IGF-1 or IGFBP-3 in SCAT of acromegaly group do not appear to contribute to systemic differences in insulin sensitivity but may have local regulatory effects in SCAT of patients with acromegaly.

Inflammation and impaired adipogenesis in hypertrophic obesity in man

2009 ◽  
Vol 297 (5) ◽  
pp. E999-E1003 ◽  
Author(s):  
Birgit Gustafson ◽  
Silvia Gogg ◽  
Shahram Hedjazifar ◽  
Lachmi Jenndahl ◽  
Ann Hammarstedt ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Subcutaneous Adipose Tissue ◽  
Molecular Mechanisms ◽  
Whole Body ◽  
Preadipocyte Differentiation ◽  
Metabolic Complications ◽  
Adipose Cell ◽  
Subcutaneous Adipose ◽  
Adipose Cell Size

Obesity is associated mainly with adipose cell enlargement in adult man (hypertrophic obesity), whereas the formation of new fat cells (hyperplastic obesity) predominates in the prepubertal age. Adipose cell size, independent of body mass index, is negatively correlated with whole body insulin sensitivity. Here, we review recent findings linking hypertrophic obesity with inflammation and a dysregulated adipose tissue, including local cellular insulin resistance with reduced IRS-1 and GLUT4 protein content. In addition, the number of preadipocytes in the abdominal subcutaneous adipose tissue capable of undergoing differentiation to adipose cells is reduced in hypertrophic obesity. This is likely to promote ectopic lipid accumulation, a well-known finding in these individuals and one that promotes insulin resistance and cardiometabolic risk. We also review recent results showing that TNFα, but not MCP-1, resistin, or IL-6, completely prevents normal adipogenesis in preadipocytes, activates Wnt signaling, and induces a macrophage-like phenotype in the preadipocytes. In fact, activated preadipocytes, rather than macrophages, may completely account for the increased release of chemokines and cytokines by the adipose tissue in obesity. Understanding the molecular mechanisms for the impaired preadipocyte differentiation in the subcutaneous adipose tissue in hypertrophic obesity is a priority since it may lead to new ways of treating obesity and its associated metabolic complications.

Visfatin mRNA expression in human subcutaneous adipose tissue is regulated by exercise

2007 ◽  
Vol 292 (1) ◽  
pp. E24-E31 ◽  
Author(s):  
Lone Frydelund-Larsen ◽  
Thorbjorn Akerstrom ◽  
Søren Nielsen ◽  
Pernille Keller ◽  
Charlotte Keller ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Mrna Expression ◽  
Subcutaneous Adipose Tissue ◽  
Recovery Period ◽  
Control Group ◽  
Time Points ◽  
Metabolic Role ◽  
Exercise Induced ◽  
Subcutaneous Adipose

Visfatin [pre-β-cell colony-enhancing factor (PBEF)] is a novel adipokine that is produced by adipose tissue, skeletal muscle, and liver and has insulin-mimetic actions. Regular exercise enhances insulin sensitivity. In the present study, we therefore examined visfatin mRNA expression in abdominal subcutaneous adipose tissue and skeletal muscle biopsies obtained from healthy young men at time points 0, 3, 4.5, 6, 9, and 24 h in relation to either 3 h of ergometer cycle exercise at 60% of V̇o2 max or rest. Adipose tissue visfatin mRNA expression increased threefold at the time points 3, 4.5, and 6 h in response to exercise ( n = 8) compared with preexercise samples and compared with the resting control group ( n = 7, P = 0.001). Visfatin mRNA expression in skeletal muscle was not influenced by exercise. The exercise-induced increase in adipose tissue visfatin was, however, not accompanied by elevated levels of plasma visfatin. Recombinant human IL-6 infusion to mimic the exercise-induced IL-6 response ( n = 6) had no effect on visfatin mRNA expression in adipose tissue compared with the effect of placebo infusion ( n = 6). The finding that exercise enhances subcutaneous adipose tissue visfatin mRNA expression suggests that visfatin has a local metabolic role in the recovery period following exercise.

scholarly journals Aerobic exercise elevates markers of angiogenesis and macrophage IL-6 gene expression in the subcutaneous adipose tissue of overweight-to-obese adults

2017 ◽  
Vol 123 (5) ◽  
pp. 1150-1159 ◽  
Author(s):  
Douglas W. Van Pelt ◽  
Lisa M. Guth ◽  
Jeffrey F. Horowitz
Keyword(s):  
Adipose Tissue ◽  
Aerobic Exercise ◽  
Mrna Expression ◽  
Subcutaneous Adipose Tissue ◽  
Acute Exercise ◽  
Whole Body ◽  
Exercise Session ◽  
Obese Adults ◽  
Important Regulator ◽  
Subcutaneous Adipose

Alterations in the inflammatory state, metabolic function, and structure of subcutaneous adipose tissue (SAT) can impact the development of insulin resistance in obesity. Exercise can improve metabolic health in obesity, but the effects of exercise on SAT are not well known. The purpose of this study was to examine the effects of acute exercise and habitual exercise training on mRNA expression of markers of lipid metabolism, inflammation, fibrosis, and hypoxia/angiogenesis in SAT, as well as adipocyte cell size. We recruited overweight-to-obese adults who exercised regularly (ACTIVE: n = 8) or were sedentary (SED: n = 12). The groups were well matched for age (27 ± 1 vs. 24 ± 2 yr), body mass index (29 ± 1 vs. 27 ± 1 kg/m2), and body composition (30 ± 1 vs. 29 ± 1% body fat), but as expected, cardiorespiratory fitness was greater in ACTIVE vs. SED (V̇o2peak: 51 ± 3 vs. 42 ± 1 ml·kg fat-free mass−1·min−1; P = 0.01). Abdominal SAT biopsy samples were obtained before and 1 h after a single session of aerobic exercise (60 min at ~65% V̇o2peak). The exercise session increased SAT mRNA expression of VEGFA, an important regulator of angiogenic processes, in both groups. In addition, SAT from ACTIVE subjects had greater mRNA expression of the endothelial cell marker CD31 compared with SED, which may be a cumulative effect of the transient increases in VEGFA with regular exercise. We also magnetically sorted CD14+ immune cells from SAT samples and found that IL-6 expression was elevated in ACTIVE compared with SED. In conclusion, exercise initiates increases in factors related to angiogenic processes and may promote alterations in macrophage inflammation in SAT. NEW & NOTEWORTHY Acute exercise in overweight/obese adults increased subcutaneous adipose tissue (SAT) mRNA expression of VEGFA, an important regulator of angiogenesis and capillary growth. In addition, subjects that regularly exercise had elevated SAT CD31 mRNA expression and elevated IL-6 mRNA in adipose tissue macrophages compared with nonexercisers. This study demonstrates that aerobic exercise may alter processes related to whole body metabolic outcomes in obesity, such as angiogenesis and immune response, in the SAT of overweight/obese adults.

scholarly journals Relationship of Total Hemoglobin in Subcutaneous Adipose Tissue with Whole-Body and Visceral Adiposity in Humans

2019 ◽  
Vol 9 (12) ◽  
pp. 2442 ◽  
Author(s):  
Miyuki Kuroiwa ◽  
Sayuri Fuse ◽  
Shiho Amagasa ◽  
Ryotaro Kime ◽  
Tasuki Endo ◽  
...  
Keyword(s):  
Risk Factors ◽  
Adipose Tissue ◽  
Body Fat ◽  
Subcutaneous Adipose Tissue ◽  
Metabolic Diseases ◽  
Visceral Adiposity ◽  
Whole Body ◽  
Visceral Fat Area ◽  
Total Hemoglobin ◽  
Subcutaneous Adipose

High whole-body and visceral adiposity are risk factors that can cause metabolic diseases. We hypothesized that the total hemoglobin concentration (total-Hb) in abdominal subcutaneous adipose tissue (SATab), an indicator of white adipose tissue (WAT) vascularity, correlates negatively with risk factors for developing metabolic diseases, such as whole-body and visceral adiposity. We tested the optical characteristics of abdominal tissue in 140 participants (45 men and 95 women) who were apparently healthy individuals with a median age of 39 years. They also had a median body fat percentage of 25.4%, a visceral fat area of 50.4 cm2, and a SATab thickness of 1.05 cm. These tests were conducted using near-infrared time-resolved spectroscopy (NIRTRS) with a 2-cm optode separation. To distinguish the segments of SATab (SegSAT) and the mixture of muscle and SATab (SegSAT+Mus), the threshold was analyzed using the slopes of (total-Hb) against the thickness of SATab using the least-squares mean method. According to the results from the logistic regression analysis, the percentage of body fat and visceral fat area remained significant predictors of the (total-Hb) (p = 0.005 and p = 0.043, respectively) in the data for SegSAT (no influence from the SATab thickness). We conclude that simple, rapid, and noninvasive NIRTRS-determined (total-Hb) in WAT could be a useful parameter for evaluating risk factors for metabolic diseases.

scholarly journals Subcutaneous Adipose Tissue Metabolic Function and Insulin Sensitivity in People with Obesity

2021 ◽  
Author(s):  
Han-Chow E. Koh ◽  
Stephan van Vliet ◽  
Terri A. Pietka ◽  
Gretchen A. Meyer ◽  
Babak Razani ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Glucose Uptake ◽  
Subcutaneous Adipose Tissue ◽  
Whole Body ◽  
Plasma Fatty Acid ◽  
Insulin Resistant ◽  
High Insulin ◽  
Subcutaneous Adipose

We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after [<sup>18</sup>F]fluorodeoxyglucose and [<sup>15</sup>O]water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. We found high insulin-stimulated whole-body glucose uptake in insulin-sensitive participants with obesity was not due to channeling of glucose into SAT, but was due to high insulin-stimulated muscle glucose uptake. Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. In addition, we observed only marginal or no differences in adipocyte size, SAT perfusion and oxygenation, and markers of SAT inflammation between insulin-resistant and insulin-sensitive obese participants. Plasma fatty acid concentration was also not different between insulin-sensitive and insulin-resistant obese participants even though SAT was resistant to the inhibitory effect of insulin on lipolysis in the insulin-resistant obese group. These data suggest several putative SAT factors that are commonly implicated in causing insulin resistance are normal consequences of SAT expansion unrelated to insulin resistance.

scholarly journals Expression of the CD11c gene in subcutaneous adipose tissue is associated with cytokine level and insulin resistance in women with polycystic ovary syndrome

2012 ◽  
Vol 167 (5) ◽  
pp. 705-713 ◽  
Author(s):  
Tao Tao ◽  
Shengxian Li ◽  
Aimin Zhao ◽  
Yanyun Zhang ◽  
Wei Liu
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Subcutaneous Adipose Tissue ◽  
Polycystic Ovary ◽  
Mrna Abundance ◽  
Model Assessment ◽  
Ovary Syndrome ◽  
Subcutaneous Adipose

Objective Alterations in the phenotypes of macrophages in adipose tissue play a key role in inflammation and insulin resistance (IR). The phenotypes of macrophages in subcutaneous adipose tissue (SAT) and the relationship between proinflammation markers and IR in women with polycystic ovary syndrome (PCOS) remain unclear. The objectives of this study are to characterize the gene expression of macrophage markers and cytokines in the SAT of PCOS women and to estimate their relationships with circulating levels of cytokines and IR. Methods The cross-sectional study involves 16 PCOS women and 18 normal control women. Cytokines and macrophage markers in the circulation and SAT were determined using ELISA, quantitative PCR, or immunofluorescence staining. IR was estimated using the homeostasis model assessment (HOMA-IR). Results The gene expression levels of CD11c along with TNF α and leptin in SAT remained significantly higher in PCOS women than in normal women (P<0.05). However, no significant differences were found in CD68 mRNA expression in SAT between women with and without PCOS (P>0.05). Furthermore, CD11c mRNA abundance provided a stronger contribution to models predicting serum levels of TNFα (sTNFα) than did CD68 mRNA abundance. Lastly, increased sTNFα was associated with increased HOMA-IR in PCOS women, and this association was independent of both overall and visceral adiposity. Conclusion The high expression level of CD11c mRNA in SAT was proved to be an important feature in PCOS women. Furthermore, CD11c mRNA abundance made a stronger contribution to models predicting sTNFα in which existing proinflammatory properties might significantly contribute to the pathogenesis of IR in PCOS women.

scholarly journals Changes in abdominal subcutaneous adipose tissue phenotype following menopause is associated with increased visceral fat mass

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Julie Abildgaard ◽  
Thorkil Ploug ◽  
Elaf Al-Saoudi ◽  
Thomas Wagner ◽  
Carsten Thomsen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Visceral Fat ◽  
Subcutaneous Adipose Tissue ◽  
Immune Cell ◽  
Whole Body ◽  
Metabolic Dysfunction ◽  
Adipocyte Hypertrophy ◽  
Subcutaneous Adipose

AbstractMenopause is associated with a redistribution of adipose tissue towards central adiposity, known to cause insulin resistance. In this cross-sectional study of 33 women between 45 and 60 years, we assessed adipose tissue inflammation and morphology in subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) across menopause and related this to menopausal differences in adipose tissue distribution and insulin resistance. We collected paired SAT and VAT biopsies from all women and combined this with anthropometric measurements and estimated whole-body insulin sensitivity. We found that menopause was associated with changes in adipose tissue phenotype related to metabolic dysfunction. In SAT, postmenopausal women showed adipocyte hypertrophy, increased inflammation, hypoxia and fibrosis. The postmenopausal changes in SAT was associated with increased visceral fat accumulation. In VAT, menopause was associated with adipocyte hypertrophy, immune cell infiltration and fibrosis. The postmenopausal changes in VAT phenotype was associated with decreased insulin sensitivity. Based on these findings we suggest, that menopause is associated with changes in adipose tissue phenotype related to metabolic dysfunction in both SAT and VAT. Whereas increased SAT inflammation in the context of menopause is associated with VAT accumulation, VAT morphology is related to insulin resistance.

scholarly journals Three Months of Regular Aerobic Exercise in Patients With Obesity Improve Systemic Subclinical Inflammation Without Major Influence on Blood Pressure and Endocrine Production of Subcutaneous Fat

2014 ◽  
pp. S299-S308 ◽  
Author(s):  
P. TRACHTA ◽  
J. DRÁPALOVÁ ◽  
P. KAVÁLKOVÁ ◽  
V. TOUŠKOVÁ ◽  
A. CINKAJZLOVÁ ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Adipose Tissue ◽  
Aerobic Exercise ◽  
Mrna Expression ◽  
Subcutaneous Adipose Tissue ◽  
Subcutaneous Fat ◽  
Control Group ◽  
Regular Exercise ◽  
Subclinical Inflammation ◽  
Subcutaneous Adipose

The aim of our study was to explore the effects of regular aerobic exercise on anthropometric, biochemical and hormonal parameters and mRNA expression of selected factors involved in metabolic regulations in subcutaneous adipose tissue of patients with obesity. Fifteen obese women with arterial hypertension underwent a three-month exercise program consisting of 30 min of aerobic exercise 3 times a week. Fifteen healthy lean women with no intervention served as a control group. Obese group underwent anthropometric measurements, blood sampling, subcutaneous adipose tissue (SCAT) biopsy and 24-h blood pressure monitoring at baseline and after three months of exercise, while control group was examined only once. At baseline, obese group had increased SCAT expression of proinflammatory cytokines and adipokines relative to control group. Three months of regular exercise improved anthropometric parameters, decreased CRP, blood glucose and HOMA-IR, while having no significant effect on lipid profile and blood pressure. Gene expressions in SCAT were not affected by physical activity with the exception of increased aquaporin-3 mRNA expression. We conclude that three months of regular exercise decrease systemic subclinical inflammation with only minor influence on the blood pressure and the endocrine function of subcutaneous fat.

Subcutaneous Adipose Tissue Metabolic Function and Insulin Sensitivity in People with Obesity

2021 ◽  
Author(s):  
Han-Chow E. Koh ◽  
Stephan van Vliet ◽  
Terri A. Pietka ◽  
Gretchen A. Meyer ◽  
Babak Razani ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Glucose Uptake ◽  
Subcutaneous Adipose Tissue ◽  
Whole Body ◽  
Plasma Fatty Acid ◽  
Insulin Resistant ◽  
High Insulin ◽  
Subcutaneous Adipose

We used stable isotope-labeled glucose and palmitate tracer infusions, a hyperinsulinemic-euglycemic clamp, positron-emission tomography of muscles and adipose tissue after [<sup>18</sup>F]fluorodeoxyglucose and [<sup>15</sup>O]water injections, and subcutaneous adipose tissue (SAT) biopsy to test the hypotheses that: i) increased glucose uptake in SAT is responsible for high insulin-stimulated whole-body glucose uptake in people with obesity who are insulin-sensitive, and ii) putative SAT factors thought to cause insulin resistance are present in people with obesity who are insulin-resistant but not in those who are insulin-sensitive. We found high insulin-stimulated whole-body glucose uptake in insulin-sensitive participants with obesity was not due to channeling of glucose into SAT, but was due to high insulin-stimulated muscle glucose uptake. Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. In addition, we observed only marginal or no differences in adipocyte size, SAT perfusion and oxygenation, and markers of SAT inflammation between insulin-resistant and insulin-sensitive obese participants. Plasma fatty acid concentration was also not different between insulin-sensitive and insulin-resistant obese participants even though SAT was resistant to the inhibitory effect of insulin on lipolysis in the insulin-resistant obese group. These data suggest several putative SAT factors that are commonly implicated in causing insulin resistance are normal consequences of SAT expansion unrelated to insulin resistance.

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