Wilkinson David, Nolting Mirjam, Mahadi Mohd Kaisan, Chapman Ian, Heilbronn Leonie
Discipline of Medicine, The University of Adelaide, Hyperbaric Medicine Unit, Royal Adelaide Hospital North Terrace, Adelaide, South Australia 5000, Australia, Phone: +61-(0)8-8222-5116, Fax: +61-(0)8-8232-4207, E-mail:
Hyperbaric Medicine Unit, Royal Adelaide Hospital, Adelaide, Australia.
Diving Hyperb Med. 2015 Mar;45(1):30-6.
The onset of insulin resistance is an important metabolic event in the development of type 2 diabetes. For patients with type 2 diabetes, we recently showed that peripheral insulin sensitivity was increased during hyperbaric oxygen treatment (HBOT). This study aims to investigate whether this occurs in a non-patient population with and without type 2 diabetes, along with the mechanism of this effect.
Overweight and obese male participants were recruited from the community, 11 without and eight with type 2 diabetes. Insulin sensitivity was measured by the glucose infusion rate (GIR) during a hyperinsulinaemic euglycaemic clamp (80 mU·m⁻²·min⁻¹) at baseline and during the third HBOT session. Monocyte chemo-attractant protein-1 (MCP-1), tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured in fasting serum and adipose tissue samples taken for their gene expression at baseline and immediately following four HBOT sessions. Additional fasting serum samples were collected during the first HBOT at 0, 60 and 120 minutes, and 24-hours after the last HBOT.
In response to HBOT, GIR was increased by 29±32% in those without (n=10, P=0.01), and by 57±66% in those with type 2 diabetes (n=7, P=0.04). This increase was maintained for 30 minutes post HBOT. Reduced MCP-1 and TNF-α were observed after HBOT, whereas IL-6 was increased only in individuals without diabetes and this correlated with the increase in insulin sensitivity (r²=0.72, P=0.004).
Peripheral insulin sensitivity was increased following HBOT in overweight or obese males with and without type 2 diabetes; this increase was maintained for at least 30 minutes post HBOT. Changes in inflammatory cytokines may partly explain this effect.
胰岛素抵抗的发生是2型糖尿病发展过程中的一个重要代谢事件。对于2型糖尿病患者，我们最近发现高压氧治疗（HBOT）期间外周胰岛素敏感性增加。本研究旨在调查在有无2型糖尿病的非患者人群中是否也会出现这种情况，以及这种效应的机制。
从社区招募超重和肥胖男性参与者，其中11人无2型糖尿病，8人患有2型糖尿病。在基线和第三次HBOT疗程期间，通过高胰岛素正常血糖钳夹试验（80 mU·m⁻²·min⁻¹）期间的葡萄糖输注率（GIR）来测量胰岛素敏感性。在基线时以及在四次HBOT疗程后立即采集空腹血清和脂肪组织样本，测量单核细胞趋化蛋白-1（MCP-1）、肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）及其基因表达。在第一次HBOT的0、60和120分钟以及最后一次HBOT后24小时收集额外的空腹血清样本。
在接受HBOT后，无2型糖尿病者（n = 10，P = 0.01）的GIR增加了29±32%，2型糖尿病患者（n = 7，P = 0.04）的GIR增加了57±66%。这种增加在HBOT后维持30分钟。HBOT后观察到MCP-1和TNF-α减少，而IL-6仅在无糖尿病个体中增加，且这与胰岛素敏感性的增加相关（r² = 0.72，P = 0.004）。
无论有无2型糖尿病，超重或肥胖男性在接受HBOT后外周胰岛素敏感性均增加；这种增加在HBOT后至少维持30分钟。炎症细胞因子的变化可能部分解释了这种效应。
