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首页> 外文期刊>The Journal of Nutritional Biochemistry >High-fat diets rich in medium- versus long-chain fatty acids induce distinct patterns of tissue specific insulin resistance.
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High-fat diets rich in medium- versus long-chain fatty acids induce distinct patterns of tissue specific insulin resistance.

机译：富含中链和长链脂肪酸的高脂饮食会引起组织特异性胰岛素抵抗的不同模式。

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摘要

Excess dietary long-chain fatty acid (LCFA) intake results in ectopic lipid accumulation and insulin resistance. Since medium-chain fatty acids (MCFA) are preferentially oxidized over LCFA, we hypothesized that diets rich in MCFA result in a lower ectopic lipid accumulation and insulin resistance compared to diets rich in LCFA. Feeding mice high-fat (HF) (45% kcal fat) diets for 8 weeks rich in triacylglycerols composed of MCFA (HFMCT) or LCFA (HFLCT) revealed a lower body weight gain in the HFMCT-fed mice. Indirect calorimetry revealed higher fat oxidation on HFMCT compared to HFLCT (0.011.0+or-0.0007 vs. 0.0096+or-0.0015 kcal/g body weight per hour, P<.05). In line with this, neutral lipid immunohistochemistry revealed significantly lower lipid storage in skeletal muscle (0.05+or-0.08 vs. 0.30+or-0.23 area%, P <.05) and in liver (0.9+or-0.4 vs. 6.4+or-0.8 area%, P<.05) after HFMCT vs. HFLCT, while ectopic fat storage in low fat (LF) was very low. Hyperinsulinemic euglycemic clamps revealed that the HFMCT and HFLCT resulted in severe whole body insulin resistance (glucose infusion rate: 53.1+or-6.8, 50.8+or-15.3 vs. 124.6+or-25.4 mumol min-1 kg-1, P<.001 in HFMCT, HFLCT and LF-fed mice, respectively). However, under hyperinsulinemic conditions, HFMCT revealed a lower endogenous glucose output (22.6+or-8.0 vs. 34.7+or-8.5 mumol min-1 kg-1, P<.05) and a lower peripheral glucose disappearance (75.7+or-7.8 vs. 93.4+or-12.4 mumol min-1 kg-1, P<.03) compared to HFLCT-fed mice. In conclusion, both HF diets induced whole body insulin resistance compared to LF. However, the HFMCT gained less weight, had less ectopic lipid accumulation, while peripheral insulin resistance was more pronounced compared to HFLCT. This suggests that HF-diets rich in medium- versus long-chain triacylglycerols induce insulin resistance via distinct mechanisms.
机译：饮食中长链脂肪酸（LCFA）摄入过多会导致异位脂质蓄积和胰岛素抵抗。由于中链脂肪酸（MCFA）比LCFA优先被氧化，因此我们假设与富含LCFA的饮食相比，富含MCFA的饮食会导致较低的异位脂质蓄积和胰岛素抵抗。饲喂富含MCFA（HFMCT）或LCFA（HFLCT）的三酰基甘油的高脂（HF）（45％kcal脂肪）高脂饮食8周显示，在以HFMCT喂养的小鼠中，体重增加较低。间接量热法显示，与HFLCT相比，HFMCT上的脂肪氧化更高（0.011.0 +或-0.0007 vs. 0.0096 +或-0.0015 kcal / g每小时体重，P <.05）。与此相符，中性脂质免疫组织化学显示骨骼肌中的脂质存储量显着降低（0.05+或-0.08对0.30+或-0.23面积％，P <.05）和肝脏（0.9+或-0.4对6.4+） HFMCT与HFLCT相比，差异为-0.8面积％，P <.05），而异位脂肪在低脂肪（LF）中的存储量非常低。高胰岛素正常血糖钳夹显示，HFMCT和HFLCT导致严重的全身胰岛素抵抗（葡萄糖输注速率：53.1+或-6.8、50.8+或-15.3与124.6+或-25.4 mumol min -1 在HFMCT，HFLCT和LF喂养的小鼠中分别为kg -1 ，P <.001）。然而，在高胰岛素条件下，HFMCT显示较低的内源性葡萄糖输出（22.6+或-8.0 vs. 34.7+或-8.5 mumol min -1 kg -1 ，P < .05）和较低的外周葡萄糖消失率（75.7 + or-7.8与93.4 + or-12.4 mumol min -1 kg -1 ，P <.03）给HFLCT喂养的小鼠。总之，与低频饮食相比，两种高频饮食都能诱导全身胰岛素抵抗。然而，与HFLCT相比，HFMCT的体重减轻，异位脂质堆积较少，而外周胰岛素抵抗更为明显。这表明富含中链和长链三酰基甘油的HF饮食通过不同的机制诱导胰岛素抵抗。

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