在犬类模型中，内脏脂肪本身的增加并不会诱发胰岛素抵抗。
Increase in visceral fat per se does not induce insulin resistance in the canine model.
作者信息
Castro Ana V B, Woolcott Orison O, Iyer Malini S, Kabir Morvarid, Ionut Viorica, Stefanovski Darko, Kolka Cathryn M, Szczepaniak Lidia S, Szczepaniak Edward W, Asare-Bediako Isaac, Paszkiewicz Rebecca L, Broussard Josiane L, Kim Stella P, Kirkman Erlinda L, Rios Hernan C, Mkrtchyan Hasmik, Wu Qiang, Ader Marilyn, Bergman Richard N
机构信息
Diabetes and Obesity Research Institute, Cedars-Sinai Medical Center, Los Angeles, California, USA.
出版信息
Obesity (Silver Spring). 2015 Jan;23(1):105-11. doi: 10.1002/oby.20906. Epub 2014 Oct 16.
OBJECTIVES
To determine whether a selective increase of visceral adipose tissue content will result in insulin resistance.
METHODS
Sympathetic denervation of the omental fat was performed under general inhalant anesthesia by injecting 6-hydroxydopamine in the omental fat of lean mongrel dogs (n = 11). In the conscious animal, whole-body insulin sensitivity was assessed by the minimal model (SI ) and the euglycemic hyperinsulinemic clamp (SICLAMP ). Changes in abdominal fat were monitored by magnetic resonance. All assessments were determined before (Wk0) and 2 weeks (Wk2) after denervation. Data are medians (upper and lower interquartile).
RESULTS
Denervation of omental fat resulted in increased percentage (and content) of visceral fat [Wk0: 10.2% (8.5-11.4); Wk2: 12.4% (10.4-13.6); P < 0.01]. Abdominal subcutaneous fat remained unchanged. However, no changes were found in SI [Wk0: 4.7 (mU/l)(-1) min(-1) (3.1-8.8); Wk2: 5.3 (mU/l)(-1) min(-1) (4.5-7.2); P = 0.59] or SICLAMP [Wk0: 42.0 × 10(-4) dl kg(-1) min(-1) (mU/l)(-1) (41.0-51.0); Wk2: 40.0 × 10(-4) dl kg(-1) min(-1) (mU/l) (-1) (34.0-52.0); P = 0.67].
CONCLUSIONS
Despite a selective increase in visceral adiposity in dogs, insulin sensitivity in vivo did not change, which argues against the concept that accumulation of visceral adipose tissue contributes to insulin resistance.
目的
确定内脏脂肪组织含量的选择性增加是否会导致胰岛素抵抗。
方法
在全身吸入麻醉下，通过向瘦杂种犬（n = 11）的网膜脂肪中注射6-羟基多巴胺来进行网膜脂肪的交感神经去神经支配。在清醒动物中，通过最小模型（SI）和正常血糖高胰岛素钳夹技术（SICLAMP）评估全身胰岛素敏感性。通过磁共振监测腹部脂肪的变化。所有评估均在去神经支配前（第0周）和去神经支配后2周（第2周）进行。数据为中位数（上下四分位数间距）。
结果
网膜脂肪去神经支配导致内脏脂肪百分比（和含量）增加[第0周：10.2%（8.5 - 11.4）；第2周：12.4%（10.4 - 13.6）；P < 0.01]。腹部皮下脂肪保持不变。然而，SI[第0周：4.7（mU/l）⁻¹ min⁻¹（3.1 - 8.8）；第2周：5.3（mU/l）⁻¹ min⁻¹（4.5 - 7.2）；P = 0.59]或SICLAMP[第0周：42.0×10⁻⁴ dl kg⁻¹ min⁻¹（mU/l）⁻¹（41.0 - 51.0）；第2周：40.0×10⁻⁴ dl kg⁻¹ min⁻¹（mU/l）⁻¹（34.0 - 52.0）；P = 0.67]均未发现变化。
结论
尽管犬内脏脂肪增多具有选择性，但体内胰岛素敏感性并未改变，这与内脏脂肪组织堆积导致胰岛素抵抗的概念相悖。
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