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Objective: We tested the hypothesis that high lipolytic responsiveness is related to increased expression of ATM genes in human adipose tissues. Design and Methods: Omental (OM) and subcutaneous (SC) fat samples were obtained surgically in 46 women (age: 47.2 6 4.7 years, BMI: 26.9 6 5.2 kg/m 2 ). Body composition and fat distribution were measured using dual energy X-ray absorptiometry and computed tomography. Lipolysis was measured by glycerol release in mature adipocytes isolated by collagenase digestion under basal-, isoproterenol (10 À5 M)-, and forskolin (10 À5 M)-stimulated conditions. Quantification of macrophage gene mRNA expression (CD11b, CD11c, and CD68) in whole adipose tissue was performed using real-time RT-PCR. Results: SC CD68 mRNA abundance was positively associated with isoproterenol-stimulated lipolysis (r ¼ 0.36, P < 0.05). This association remained significant after adjustment for total body fat mass (r ¼ 0.34, P 0.05). In the OM depot, CD11b mRNA abundance was positively associated with isoproterenol-stimulated lipolysis (r ¼ 0.42, P 0.005). This association remained significant after adjustment for total body fat mass (r ¼ 0.41, P 0.01). In subgroup analyses, high lipolytic rates in SC adipocytes were related to increased whole tissue expression of CD68 and CD11b in this compartment, independent of adiposity and fat cell size (P 0.001 and P 0.05). High lipolytic rates in OM adipocytes were related to increased whole tissue OM expression of CD11b, independent of adiposity and fat cell size (P 0.05). Conclusions: High adipocyte lipolytic responsiveness is related to increased expression of ATM markers in the corresponding compartment, independent of adiposity and fat cell size.
Objective: We tested the hypothesis that high lipolytic responsiveness is related to increased expression of ATM genes in human adipose tissues. Design and Methods: Omental (OM) and subcutaneous (SC) fat samples were obtained surgically in 46 women (age: 47.2 6 4.7 years, BMI: 26.9 6 5.2 kg/m 2 ). Body composition and fat distribution were measured using dual energy X-ray absorptiometry and computed tomography. Lipolysis was measured by glycerol release in mature adipocytes isolated by collagenase digestion under basal-, isoproterenol (10 À5 M)-, and forskolin (10 À5 M)-stimulated conditions. Quantification of macrophage gene mRNA expression (CD11b, CD11c, and CD68) in whole adipose tissue was performed using real-time RT-PCR. Results: SC CD68 mRNA abundance was positively associated with isoproterenol-stimulated lipolysis (r ¼ 0.36, P < 0.05). This association remained significant after adjustment for total body fat mass (r ¼ 0.34, P 0.05). In the OM depot, CD11b mRNA abundance was positively associated with isoproterenol-stimulated lipolysis (r ¼ 0.42, P 0.005). This association remained significant after adjustment for total body fat mass (r ¼ 0.41, P 0.01). In subgroup analyses, high lipolytic rates in SC adipocytes were related to increased whole tissue expression of CD68 and CD11b in this compartment, independent of adiposity and fat cell size (P 0.001 and P 0.05). High lipolytic rates in OM adipocytes were related to increased whole tissue OM expression of CD11b, independent of adiposity and fat cell size (P 0.05). Conclusions: High adipocyte lipolytic responsiveness is related to increased expression of ATM markers in the corresponding compartment, independent of adiposity and fat cell size.
Obesity is a chronic condition involving inflammation and oxidative stress that commonly predisposes affected individuals to develop metabolic disorders. We hypothesize that Ilex paraguariensis (IP) can modulate oxidative stress and inflammation underpinning metabolic disorders caused by obesity. C57BL/6 mice were fed a high‐fat diet (HFD group) for 12 weeks. Concomitantly, some mice were treated with roasted IP (15 mg/ml – HFD + IP) or dimethyl fumarate (DMF) as a positive control (2 mg/ml – HFD + DMF). The control group received standard chow and water ad libitum. Histological analyses of fat tissue and liver, and quantification of mediators related to oxidative stress (Kelch‐like ECH‐associated protein 1/NF‐E2‐related factor 2, NADP(H) quinone oxidoreductase‐1 [NQO1], heme oxygenase 1 [HO1], and superoxide dismutase) as well as metabolic profile blood biomarkers (glucose, leptin, resistin, high‐density lipoproteins [HDLs], and triglycerides) were performed. Metabolic disorders were prevented in mice treated with IP, as evidenced by the observation that glucose, HDL, and resistin levels were similar to those assessed in the control group. Morphological analyses showed that both IP and DMF treatments prevented hepatic steatosis and adipocyte hypertrophy in visceral adipose tissue. Finally, although the antioxidant response stimulated by IP was quite limited, significant effects were found on NQO1 and HO1 expression. In conclusion, IP has promising preventative effects on the development of metabolic disorders caused by obesity.
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