Abstract：
OBJECTIVE: To examine the impact of impaired glycaemic regulation (IGR) and exercise training on hepatic lipid composition in men with metabolic dysfunction-associated steatotic liver disease (MASLD).
METHODS: In Part A (cross-sectional design), 40 men with MASLD (liver proton density fat fraction [PDFF] ≥5.56%) were recruited to one of two groups: (1) normal glycaemic regulation (NGR) group (glycated haemoglobin [HbA1c] < 42 mmol∙mol-1 [<6.0%]; n = 14) or (2) IGR group (HbA1c ≥ 42 mmol∙mol-1 [≥6.0%]; n = 26). In Part B (randomized controlled trial design), participants in the IGR group were randomized to one of two 6-week interventions: (1) exercise training (EX; 70%-75% maximum heart rate; four sessions/week; n = 13) or (2) non-exercise control (CON; n = 13). Saturated (SI; primary outcome), unsaturated (UI) and polyunsaturated (PUI) hepatic lipid indices were determined using proton magnetic resonance spectroscopy. Additional secondary outcomes included liver PDFF, HbA1c, fasting plasma glucose (FPG), homeostatic model assessment of insulin resistance (HOMA-IR), peak oxygen uptake (VO2 peak), and plasma cytokeratin-18 (CK18) M65, among others.
RESULTS: In Part A, hepatic SI was higher and hepatic UI was lower in the IGR versus the NGR group (p = 0.038), and this hepatic lipid profile was associated with higher HbA1c levels, FPG levels, HOMA-IR and plasma CK18 M65 levels (rs ≥0.320). In Part B, hepatic lipid composition and liver PDFF were unchanged after EX versus CON (p ≥ 0.257), while FPG was reduced and VO2 peak was increased (p ≤ 0.030). ΔVO2 peak was inversely associated with Δhepatic SI (r = -0.433) and positively associated with Δhepatic UI and Δhepatic PUI (r ≥ 0.433).
CONCLUSIONS: Impaired glycaemic regulation in MASLD is characterized by greater hepatic lipid saturation; however, this composition is not altered by 6 weeks of moderate-intensity exercise training.
METHODS: In Part A (cross-sectional design), 40 men with MASLD (liver proton density fat fraction [PDFF] ≥5.56%) were recruited to one of two groups: (1) normal glycaemic regulation (NGR) group (glycated haemoglobin [HbA1c] < 42 mmol∙mol-1 [<6.0%]; n = 14) or (2) IGR group (HbA1c ≥ 42 mmol∙mol-1 [≥6.0%]; n = 26). In Part B (randomized controlled trial design), participants in the IGR group were randomized to one of two 6-week interventions: (1) exercise training (EX; 70%-75% maximum heart rate; four sessions/week; n = 13) or (2) non-exercise control (CON; n = 13). Saturated (SI; primary outcome), unsaturated (UI) and polyunsaturated (PUI) hepatic lipid indices were determined using proton magnetic resonance spectroscopy. Additional secondary outcomes included liver PDFF, HbA1c, fasting plasma glucose (FPG), homeostatic model assessment of insulin resistance (HOMA-IR), peak oxygen uptake (VO2 peak), and plasma cytokeratin-18 (CK18) M65, among others.
RESULTS: In Part A, hepatic SI was higher and hepatic UI was lower in the IGR versus the NGR group (p = 0.038), and this hepatic lipid profile was associated with higher HbA1c levels, FPG levels, HOMA-IR and plasma CK18 M65 levels (rs ≥0.320). In Part B, hepatic lipid composition and liver PDFF were unchanged after EX versus CON (p ≥ 0.257), while FPG was reduced and VO2 peak was increased (p ≤ 0.030). ΔVO2 peak was inversely associated with Δhepatic SI (r = -0.433) and positively associated with Δhepatic UI and Δhepatic PUI (r ≥ 0.433).
CONCLUSIONS: Impaired glycaemic regulation in MASLD is characterized by greater hepatic lipid saturation; however, this composition is not altered by 6 weeks of moderate-intensity exercise training.
摘要：
目的：研究血糖调节受损（IGR）和运动训练对代谢功能障碍相关脂肪变性肝病（MASLD）男性肝脏脂质组成的影响。
方法：在A部分（横截面设计）中，将40名MASLD（肝脏质子密度脂肪分数[PDFF]≥5.56％）的男性纳入两组之一：（1）正常血糖调节（NGR）组（糖化血红蛋白[HbA1c]<42mmol·mol-1[<6.0％]；n=14）或（2）IGR组（HbA1c≥42mmol·mol-1[≥6.0％]；n=26）。在B部分(随机对照试验设计)中，IGR组的参与者被随机分配到两个为期6周的干预措施中的一个:(1)运动训练(EX;最大心率70%~75%;每周4次;n=13)或(2)非运动控制(CON;n=13).饱和（SI；主要结果），使用质子磁共振波谱测定不饱和（UI）和多不饱和（PUI）肝脂质指数。其他次要结果包括肝脏PDFF，HbA1c,空腹血糖（FPG），胰岛素抵抗的稳态模型评估（HOMA-IR），峰值摄氧量（VO2峰值），和血浆细胞角蛋白-18(CK18)M65等。
结果：在A部分中，与NGR组相比，IGR组的肝SI较高，肝UI较低（p=0.038），这种肝脏脂质分布与较高的HbA1c水平有关，FPG水平,HOMA-IR和血浆CK18M65水平（rs≥0.320）。在B部分,与CON相比，EX后的肝脏脂质成分和肝脏PDFF没有变化（p≥0.257），FPG降低，VO2峰值增加（p≤0.030）。ΔVO2峰与Δ肝SI呈负相关（r=-0.433），与Δ肝UI和Δ肝PUI呈正相关（r≥0.433）。
结论：MASLD中的血糖调节受损的特征是肝脏脂质饱和度较高；然而，6周的中等强度运动训练不会改变这种成分。
方法：在A部分（横截面设计）中，将40名MASLD（肝脏质子密度脂肪分数[PDFF]≥5.56％）的男性纳入两组之一：（1）正常血糖调节（NGR）组（糖化血红蛋白[HbA1c]<42mmol·mol-1[<6.0％]；n=14）或（2）IGR组（HbA1c≥42mmol·mol-1[≥6.0％]；n=26）。在B部分(随机对照试验设计)中，IGR组的参与者被随机分配到两个为期6周的干预措施中的一个:(1)运动训练(EX;最大心率70%~75%;每周4次;n=13)或(2)非运动控制(CON;n=13).饱和（SI；主要结果），使用质子磁共振波谱测定不饱和（UI）和多不饱和（PUI）肝脂质指数。其他次要结果包括肝脏PDFF，HbA1c,空腹血糖（FPG），胰岛素抵抗的稳态模型评估（HOMA-IR），峰值摄氧量（VO2峰值），和血浆细胞角蛋白-18(CK18)M65等。
结果：在A部分中，与NGR组相比，IGR组的肝SI较高，肝UI较低（p=0.038），这种肝脏脂质分布与较高的HbA1c水平有关，FPG水平,HOMA-IR和血浆CK18M65水平（rs≥0.320）。在B部分,与CON相比，EX后的肝脏脂质成分和肝脏PDFF没有变化（p≥0.257），FPG降低，VO2峰值增加（p≤0.030）。ΔVO2峰与Δ肝SI呈负相关（r=-0.433），与Δ肝UI和Δ肝PUI呈正相关（r≥0.433）。
结论：MASLD中的血糖调节受损的特征是肝脏脂质饱和度较高；然而，6周的中等强度运动训练不会改变这种成分。
