Overfeeding energy upregulates peroxisome proliferator-activated receptor (PPAR)γ-controlled adipogenic and lipolytic gene networks but does not affect proinflammatory markers in visceral and subcutaneous adipose depots of Holstein cows.
Overfeeding energy upregulates peroxisome proliferator-activated receptor (PPAR)γ-controlled adipogenic and lipolytic gene networks but does not affect proinflammatory markers in visceral and subcutaneous adipose depots of Holstein cows.
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过度饲喂能量会上调过氧化物酶体增殖物激活受体（PPAR）γ控制的脂肪形成和脂肪分解基因网络，但不影响荷斯坦奶牛内脏和皮下脂肪库中的促炎标志物。
作者：
P. Ji;J. Drackley;M. J. Khan;J. Loor
我们的目的是确定过度饲喂能量对非妊娠和非泌乳荷斯坦奶牛肠系膜 (MAT)、网膜 (OAT) 和皮下 (SAT) 脂肪组织 (AT) 基因表达的影响。 18 头奶牛被随机分配为低能量 [LE，泌乳净能量 (NE(L)) = 1.35 Mcal/kg 干物质 (DM)] 或高能量（HE，NE(L) = 1.62 Mcal/kg DM）日粮，为期 8 周。然后对奶牛实施安乐死，并收集 MAT、OAT 和 SAT 的子样本，通过对参与脂肪生成、三酰甘油 (TAG) 合成、脂肪分解、乳酸信号传导、转录调控和炎症的 34 个基因进行定量 PCR 进行转录谱分析。膳食能量和 AT 库的相互作用仅对 LPL 显着，这表明 3 个位点之间的反应一致。与 LE 相比，HE 上调了与脂肪酸从头合成 (FASN) 和去饱和 (SCD) 相关的关键基因的表达。与这些过程相关的其他基因，如 ACLY、ACACA、ELOVL6、FABP4、GPAM 和 LPIN1，在 HE 的数值上上调。与 LE 相比，HE 的脂解基因（PNPLA2 和 ABHD5）表达上调，抗脂解乳酸受体 HCAR1 下调。 HE 上调假定的转录调节因子 THRSP，转录调节因子 PPARG 上调，而 SREBF1 下调。在脂肪细胞因子中，HE倾向于上调CCL2的表达，而IL6R则下调。总体而言，结果表明，过度喂食能量可能至少部分通过刺激包含与从头合成相关的关键基因的网络转录来增加 AT 质量。为了应对能量过度喂养，PPARG 而不是 SREBF1 的表达与大多数脂肪形成或脂肪生成基因密切相关。然而，这些调节因子的转录活性需要得到验证，以确认它们在牛 AT 脂肪生成或脂肪生成调节中的作用。过度饲喂能量还可能通过刺激 TAG 水解基因的表达，同时抑制羟基羧酸受体 (HCAR1)（一种新型抗脂肪分解调节剂）的信号传导，使奶牛具有更大的脂肪分解潜力。我们的结果并不支持脂肪组织因 8 周能量过量喂养而出现明显的炎症反应。
Our objective was to determine the effects of overfeeding energy on gene expression in mesenteric (MAT), omental (OAT), and subcutaneous (SAT) adipose tissue (AT) from nonpregnant and nonlactating Holstein cows. Eighteen cows were randomly assigned to either a low energy [LE, net energy for lactation (NE(L)) = 1.35 Mcal/kg of dry matter (DM)] or high energy (HE, NE(L) = 1.62 Mcal/kg of DM) diets for 8 wk. Cows were then euthanized and subsamples of MAT, OAT, and SAT were harvested for transcript profiling via quantitative PCR of 34 genes involved in lipogenesis, triacylglycerol (TAG) synthesis, lipolysis, lactate signaling, transcription regulation, and inflammation. The interaction of dietary energy and AT depot was only significant for LPL, which indicated a consistent response among the 3 sites. The expression of key genes related to de novo fatty acid synthesis (FASN) and desaturation (SCD) was upregulated by HE compared with LE. Other genes associated with those processes, such as ACLY, ACACA, ELOVL6, FABP4, GPAM, and LPIN1, were numerically upregulated by HE. The expression of lipolytic (PNPLA2 and ABHD5) genes was upregulated and the antilypolytic lactate receptor HCAR1 was downregulated with HE compared with LE. The putative transcription regulator THRSP was upregulated and the transcription regulator PPARG tended to be upregulated by HE, whereas SREBF1 was downregulated. Among adipocytokines, HE tended to upregulate the expression of CCL2, whereas IL6R was downregulated. Overall, results indicated that overfeeding energy may increase AT mass at least in part by stimulating transcription of the network encompassing key genes associated with de novo synthesis. In response to energy overfeeding, the expression of PPARG rather than SREBF1 was closely associated with most adipogenic or lipogenic genes. However, the transcriptional activity of these regulators needs to be verified to confirm their role in the regulation of adipogenesis or lipogenesis in bovine AT. Overfeeding energy also may predispose cows to greater lipolytic potential by stimulating expression of TAG hydrolysis genes while inhibiting signaling via hydroxycarboxylic acid receptor (HCAR1), which is a novel antilipolytic regulator. Our results do not support an overt inflammatory response in adipose tissues in response to an 8-wk energy overfeeding.
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DOI：
10.1016/j.bbrc.2012.07.082
发表时间：
2012-08-24
影响因子：
3.1
作者：
Wanders, Desiree;Graff, Emily C.;Judd, Robert L.
通讯作者：
Judd, Robert L.
DOI：
10.1172/jci15593
发表时间：
2002-05
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
J. Horton;J. Goldstein;Michael S. Brown
通讯作者：
J. Horton;J. Goldstein;Michael S. Brown
脂肪酸结合蛋白的小分子抑制剂的鉴定和表征。
影响因子：
7.3
作者：
Hertzel AV;Hellberg K;Reynolds JM;Kruse AC;Juhlmann BE;Smith AJ;Sanders MA;Ohlendorf DH;Suttles J;Bernlohr DA
通讯作者：
Bernlohr DA
影响因子：
10.5
作者：
Lefterova, Martina I.;Zhang, Yong;Lazar, Mitchell A.
通讯作者：
Lazar, Mitchell A.
DOI：
10.1073/pnas.96.10.5528
发表时间：
1999-05-11
影响因子：
11.1
作者：
Shen, WJ;Sridhar, K;Kraemer, FB
通讯作者：
Kraemer, FB