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.

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.

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.

Thermogenic response to epinephrine in the forearm and abdominal subcutaneous adipose tissue

1992 ◽  
Vol 263 (5) ◽  
pp. E850-E855 ◽  
Author(s):  
L. Simonsen ◽  
J. Bulow ◽  
J. Madsen ◽  
N. J. Christensen
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Oxygen Uptake ◽  
Glucose Uptake ◽  
Subcutaneous Adipose Tissue ◽  
Whole Body ◽  
Epinephrine Infusion ◽  
Basal Period ◽  
Subcutaneous Adipose

Whole body energy expenditure, thermogenic and metabolic changes in the forearm, and intercellular glucose concentrations in subcutaneous adipose tissue on the abdomen determined by microdialysis were measured during epinephrine infusion in healthy subjects. After a control period, epinephrine was infused at rates of 0.2 and 0.4 nmol.kg-1 x min-1. Whole body resting energy expenditure was 4.36 +/- 0.56 (SD) kJ/min. Energy expenditure increased to 5.14 +/- 0.74 and 5.46 +/- 0.79 kJ/min, respectively (P < 0.001), during the epinephrine infusions. Respiratory exchange ratio was 0.80 +/- 0.04 in the resting state and did not change. Local forearm oxygen uptake was 3.9 +/- 1.3 mumol.100 g-1 x min-1 in the basal period. During epinephrine infusion, it increased to 5.8 +/- 2.1 (P < 0.03) and 7.5 +/- 2.3 mumol.100 g-1 x min-1 (P < 0.001). Local forearm glucose uptake was 0.160 +/- 0.105 mumol.100 g-1 x min-1 and increased to 0.586 +/- 0.445 and 0.760 +/- 0.534 mumol.100 g-1 x min-1 (P < 0.025). The intercellular glucose concentration in the subcutaneous adipose tissue on the abdomen was equal to the arterial concentration in the basal period but did not increase as much during infusion of epinephrine, indicating glucose uptake in adipose tissue in this condition. If it is assumed that forearm skeletal muscle is representative for the average skeletal muscle, it can be calculated that on average 40% of the enhanced whole body oxygen uptake induced by infusion of epinephrine is taking place in skeletal muscle. It is proposed that adipose tissue may contribute to epinephrine-induced thermogenesis.

scholarly journals Increased Subcutaneous Adipose Tissue Expression of Genes Involved in Glycerolipid-Fatty Acid Cycling in Obese Insulin-Resistant Versus -Sensitive Individuals

2014 ◽  
Vol 99 (12) ◽  
pp. E2518-E2528 ◽  
Author(s):  
Marie-Soleil Gauthier ◽  
Joelle R. Pérusse ◽  
Marie-Ève Lavoie ◽  
Robert Sladek ◽  
S. R. Murthy Madiraju ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Subcutaneous Adipose Tissue ◽  
Tissue Expression ◽  
Insulin Resistant ◽  
Expression Of Genes ◽  
Subcutaneous Adipose

scholarly journals Four‑Stage Evolution of Diabetes or Whole Body Insulin Resistance (WBIR): Debunking of the Lipid‑Induced Insulin Resistance (LIIR) and Proposing of the Glycation‑Induced Insulin Resistance (GIIR)

2019 ◽  
Author(s):  
Song Jae Lee ◽  
Sang Won Shin
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Glucose Uptake ◽  
Hepatic Insulin Resistance ◽  
Whole Body ◽  
Rapid Weight Loss ◽  
Global Parameter ◽  
Tissue Specific ◽  
Visceral Adipose ◽  
Subcutaneous Adipose

Even though it has long been known that diabetes develops in distinctive stages over a long span of time, no comprehensive diabetes development model has been developed yet. Insulin resistance (IR) plays a major role in development of diabetes. A widespread belief regarding IR is that it is a global parameter affecting the whole body simultaneously by merely impairing glucose uptake in tissues. However, investigation by a new methodology that we have named integrated approach suggests that IR not merely impairs glucose uptake in tissues but also produces tissue‑specific metabolic disruptions varying widely from tissue to tissue, and that IR would not necessarily develop simultaneously over the whole body but instead develop first preferentially in the muscle tissue with a relatively low cell turnover and then progresses in sequence to the subcutaneous adipose tissue to the visceral adipose tissue to the liver with higher cell turnovers. This is the most important rationale for subdividing IR into the four distinct tissue‑specific IRs: muscle insulin resistance (MIR), subcutaneous adipose insulin resistance (s‑AIR), visceral adipose insulin resistance (v‑AIR), and hepatic insulin resistance (HIR). Sequential development of tissue‑specific IRs, in the order of MIR, s‑AIR, v‑AIR, and HIR, producing tissue‑specific metabolic disruptions is nothing but the whole body insulin resistance (WBIR) evolving in four distinctively insulin‑resistant stages. Four‑stage evolution from rapid weight gain to visceral obesity to rapid weight loss to full‑blown diabetic state not only complies well with the natural development history of diabetes, but also resolves most of controversies on diabetes or obesity. Development of the four‑stage WBIR evolution model, which also refutes the entrenched notion of the lipid‑induced insulin resistance (LIIR) but instead supports the glycation‑induced insulin resistance (GIIR) proposed in this study, may possibly be considered a breakthrough in study of diabetes or obesity.

Effect of training on insulin sensitivity of glucose uptake and lipolysis in human adipose tissue

2000 ◽  
Vol 279 (2) ◽  
pp. E376-E385 ◽  
Author(s):  
Bente Stallknecht ◽  
Jens J. Larsen ◽  
Kari J. Mikines ◽  
Lene Simonsen ◽  
Jens Bülow ◽  
...  
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Subcutaneous Adipose Tissue ◽  
Whole Body ◽  
Tissue Blood Flow ◽  
Glycerol Concentration ◽  
Adipose Tissue Blood Flow ◽  
Subcutaneous Adipose

Training increases insulin sensitivity of both whole body and muscle in humans. To investigate whether training also increases insulin sensitivity of adipose tissue, we performed a three-step hyperinsulinemic, euglycemic clamp in eight endurance-trained (T) and eight sedentary (S) young men [insulin infusion rates: 10,000 ( step I), 20,000 ( step II), and 150,000 ( step III) μU · min−1 · m−2]. Glucose and glycerol concentrations were measured in arterial blood and also by microdialysis in interstitial fluid in periumbilical, subcutaneous adipose tissue and in quadriceps femoris muscle (glucose only). Adipose tissue blood flow was measured by 133Xe washout. In the basal state, adipose tissue blood flow tended to be higher in T compared with S subjects, and in both groups blood flow was constant during the clamp. The change from basal in arterial-interstitial glucose concentration difference was increased in T during the clamp but not in S subjects in both adipose tissue and muscle [adipose tissue: step I ( n = 8), 0.48 ± 0.18 mM (T), 0.23 ± 0.11 mM (S); step II ( n = 8), 0.19 ± 0.09 (T), −0.09 ± 0.24 (S); step III( n = 5), 0.47 ± 0.24 (T), 0.06 ± 0.28 (S); (T: P < 0.001, S: P > 0.05); muscle: step I ( n = 4), 1.40 ± 0.46 (T), 0.31 ± 0.21 (S); step II ( n = 4), 1.14 ± 0.54 (T), −0.08 ± 0.14 (S); step III( n = 4), 1.23 ± 0.34 (T), 0.24 ± 0.09 (S); (T: P < 0.01, S: P > 0.05)]. Interstitial glycerol concentration decreased faster in T than in S subjects [half-time: T, 44 ± 9 min ( n = 7); S, 102 ± 23 min ( n = 5); P < 0.05]. In conclusion, training enhances insulin sensitivity of glucose uptake in subcutaneous adipose tissue and in skeletal muscle. Furthermore, interstitial glycerol data suggest that training also increases insulin sensitivity of lipolysis in subcutaneous adipose tissue. Insulin per se does not influence subcutaneous adipose tissue blood flow.

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 Four‑Stage Evolution of Diabetes or Whole Body Insulin Resistance (WBIR): Debunking of the Lipid‑Induced Insulin Resistance (LIIR) and Proposing of the Glycation‑Induced Insulin Resistance (GIIR)

2019 ◽  
Author(s):  
Song Jae Lee ◽  
Sang Won Shin
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Glucose Uptake ◽  
Hepatic Insulin Resistance ◽  
Whole Body ◽  
Rapid Weight Loss ◽  
Global Parameter ◽  
Tissue Specific ◽  
Visceral Adipose ◽  
Subcutaneous Adipose

Even though it has long been known that diabetes develops in distinctive stages over a long span of time, no comprehensive diabetes development model has been developed yet. Insulin resistance (IR) plays a central role in development of diabetes. A widespread belief regarding IR is that it is a global parameter affecting the whole body simultaneously by impairing merely glucose uptake in tissues. However, the analysis by a new methodology that we have named integrated approach suggests that IR not merely impairs glucose uptake in tissues but also produces tissue-specific metabolic disruptions varying widely from tissue to tissue, and that IR would not necessarily develop simultaneously over the whole body but instead develop first preferentially in the muscle tissue with a relatively low cell turnover and then progress in sequence to the subcutaneous adipose tissue to the visceral adipose tissue to the liver with higher cell turnovers. This is the most important rationale for subdividing IR into four distinct tissue-specific IRs: muscle insulin resistance (MIR), subcutaneous adipose insulin resistance (s-AIR), visceral adipose insulin resistance (v-AIR), and hepatic insulin resistance (HIR). Sequential development of tissue-specific IRs, in the order of MIR, s-AIR, v-AIR, and HIR, producing tissue-specific metabolic disruptions, is nothing but the whole body insulin resistance (WBIR) evolving in four distinctively insulin-resistant stages. Four-stage evolution from rapid weight gain to visceral obesity to rapid weight loss to full-blown diabetic state not only complies well with the natural development history of diabetes, but also resolves most of controversies on diabetes or obesity. Development of the four-stage WBIR evolution model, which also refutes the entrenched notion of the lipid-induced insulin resistance (LIIR) but instead supports the glycation-induced insulin resistance (GIIR) proposed in this study, may possibly be considered a breakthrough in study of diabetes as well as obesity.

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.

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