Morphological Characteristics of Abdominal Adipose Tissue in Normal-Weight and Obese Women of Different Metabolic Profiles

Srdić, Biljana; Stokić, Edita; Korać, Aleksandra; Ukropina, Mirela; Veličković, Ksenija; Breberina, M

doi:10.1055/s-0030-1254165

Cited by 26 publications

(26 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This finding agrees with previous studies [33, 36, 47–49], although most reports of MHO do not find significant differences in age between healthy and unhealthy obese groups [3, 12, 13, 15, 19, 34, 35, 38, 41, 43, 50–64]. A few studies have even documented significantly older MHO groups [21, 42, 65].…”

Section: Discussionsupporting

confidence: 92%

“…(Although not reported here, the current analysis also used ≤1 ATP-III criteria as the definition of metabolic health; the same pattern of results was found.) The specific combined definition used here was chosen from many definitions that combined a marker of insulin resistance with metabolic syndrome-type criteria and because it was the most frequently applied combined definition in the literature [7, 24, 35, 36]. …”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

All-Cause Mortality Risk of Metabolically Healthy Obese Individuals in NHANES III

2012

View full text Add to dashboard Cite

Mortality risk across metabolic health-by-BMI categories in NHANES-III was examined. Metabolic health was defined as: (1) homeostasis model assessment-insulin resistance (HOMA-IR) <2.5; (2) ≤2 Adult Treatment Panel (ATP) III metabolic syndrome criteria; (3) combined definition using ≤1 of the following: HOMA-IR ≥1.95 (or diabetes medications), triglycerides ≥1.7 mmol/L, HDL-C <1.04 mmol/L (males) or <1.30 mmol/L (females), LDL-C ≥2.6 mmol/L, and total cholesterol ≥5.2 mmol/L (or cholesterol-lowering medications). Hazard ratios (HR) for all-cause mortality were estimated with Cox regression models. Nonpregnant women and men were included (n = 4373, mean ± SD, age 37.1 ± 10.9 years, BMI 27.3 ± 5.8 kg/m2, 49.4% female). Only 40 of 1160 obese individuals were identified as MHO by all definitions. MHO groups had superior levels of clinical risk factors compared to unhealthy individuals but inferior levels compared to healthy lean groups. There was increased risk of all-cause mortality in metabolically unhealthy obese participants regardless of definition (HOMA-IR HR 2.07 (CI 1.3–3.4), P < 0.01; ATP-III HR 1.98 (CI 1.4–2.9), P < 0.001; combined definition HR 2.19 (CI 1.3–3.8), P < 0.01). MHO participants were not significantly different from healthy lean individuals by any definition. While MHO individuals are not at significantly increased risk of all-cause mortality, their clinical risk profile is worse than that of metabolically healthy lean individuals.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

All-Cause Mortality Risk of Metabolically Healthy Obese Individuals in NHANES III

2012

View full text Add to dashboard Cite

show abstract

“…To add to these results, no significant relationship was found between OM FCS and HOMA-IR in non-diabetic obese adults, yet OM FCS was associated with these variables independently of BMI and WHR in vitro when glucose uptake in freshly isolated adipocytes stimulated by insulin was measured 24 . In morbidly obese patients with insulin resistance, a greater proportion of adipocytes exceeding 100 mm diameter was also observed along with a lower proportion of small adipocytes compared to insulin sensitive patients 7,52,64 . This relation was challenged recently by van Beek and colleagues 65 , who reported no difference in adipocyte size between subjects with T2DM compared to those with NGT.…”

Section: Glucose Homeostasis Insulin Resistance and T2dmmentioning

confidence: 92%

Adipocyte size as a determinant of metabolic disease and adipose tissue dysfunction

Laforest¹,

Labrecque²,

Michaud³

et al. 2015

Critical Reviews in Clinical Laboratory Sciences

186

148

View full text Add to dashboard Cite

Obesity is a heterogeneous disease and is associated with comorbidities such as type 2 diabetes mellitus, cardiovascular disease and cancer. Several studies have examined the role of dysfunctional adipose tissue in the pathogenesis of obesity, highlighting the contrasting properties and impact of distinct fat compartments, sometimes with contradictory results. Dysfunctional adipose tissue involves enlargement, or hypertrophy, of pre-existing fat cells, which is thought to confer increases in cardiometabolic risk, independent of the level of obesity per se. In this article, we critically analyze available literature that examined the ability of adipocyte cell size to predict metabolic disease and adipose tissue dysfunction in humans. Many studies demonstrate that increased fat cell size is a significant predictor of altered blood lipid profiles and glucose-insulin homeostasis independent of adiposity indices. The contribution of visceral adiposity to these associations appears to be of particular importance. However, available studies are not unanimous and many fat depot-specific aspects of the relationship between increased fat cell size and cardiometabolic risk or parameters of adipose tissue dysfunction are still unresolved. Methodological factors such as the approach used to express the data may represent significant confounders in these studies. Additional studies should consider the fact that the relationship between fat cell size and common adiposity indices is non-linear, particularly when reaching the obese range. In conclusion, our analysis demonstrates that fat cell size is a significant predictor of the cardiometabolic alterations related to obesity. We propose that adipocyte hypertrophy, especially in the visceral fat compartment, may represent a strong marker of limited hyperplasic capacity in subcutaneous adipose tissues, which in turn is associated with the presence of numerous cardiometabolic alterations.

show abstract

“…Dysfunctional adipose tissue changes its standard endocrine pattern decreasing production of "defensive" adipokines such as adiponectin, and increasing secretion of "offensive" adipokines with pro-inflammatory, diabetogenic and proatherogenic properties [15][16][17][18][19][20][21]. The majority of pro-inflammatory adipokines is product of immune cells that populate adipose tissue [22].…”

Section: Dysfunctional Adipose Tissuementioning

confidence: 99%

“…Basically, obesity-linked complications can be considered as the result of the imbalance between pro-and anti-inflammatory adipokines. Hypoxia has been designated to be the key factor in the dysregulation of adipose tissue function; it induces secretion of key inflammation-related adipokines, including leptin and interleukin 6 (IL-6), and inhibits secretion of adiponectin which has anti-inflammatory and insulin-sensitising properties [13,19,[23][24][25].…”

Section: Dysfunctional Adipose Tissuementioning

confidence: 99%

Influence of Vitamin D Deficiency on Cardiometabolic Risk in Obesity

Stokić¹,

Hakkak²,

Romani³

et al. 2017

J Obes Chronic Dis

View full text Add to dashboard Cite

Morphological Characteristics of Abdominal Adipose Tissue in Normal-Weight and Obese Women of Different Metabolic Profiles

Abstract: Changes in adipocyte size, cellular and vascular density of adipose tissue in relation with metabolic disorders, regardless of nutritional level, suggest limited capacity of fat deposition and adipose tissue response to hypoxia.

Cited by 26 publications

References 20 publications

All-Cause Mortality Risk of Metabolically Healthy Obese Individuals in NHANES III

All-Cause Mortality Risk of Metabolically Healthy Obese Individuals in NHANES III

Adipocyte size as a determinant of metabolic disease and adipose tissue dysfunction

Influence of Vitamin D Deficiency on Cardiometabolic Risk in Obesity

Contact Info

Product

Resources

About