Key result
Diaphragm active-force was significantly higher in fatty rats (96±7 mN.mm-2) compared with controls (84±8 mN.mm-2, P=0.02), but not in diabetic fatty rats (90±17 mN.mm-2).
Why the study?
Does obesity or diabetic obesity improve diaphragmatic function in a rat model?
Does obesity or diabetic obesity improve diaphragmatic function in a rat model?
Absolute Event Rate: 96% vs 84%
p-value: p=0.02
Diaphragmatic force is paradoxically increased in obese rats before and after mechanical ventilation, potentially providing a physiological basis for the 'obesity paradox' observed in ICU patients.
Rodent obesity-diabetes diaphragm findings warrant clinical caution; hypothesis-generating and leaves open human translation.
BACKGROUND: Obesity is associated with a decrease in mortality in the intensive care unit (ICU) (the "obesity paradox"). We hypothesized that obesity may paradoxically improve diaphragmatic function. METHODS: Diaphragm contractility was prospectively recorded in vitro in adult male Zucker lean (control), fatty, and diabetic fatty rats, at rest, after 12h mechanical ventilation and after fatigue. We analyzed diaphragm morphology, cytokines, and protein expression of the protein kinase signaling pathways. RESULTS: Diaphragm active-force (AF) was higher in fatty (96±7mN.mm-2,P = 0.02) but not in diabetic fatty rats (90±17mN.mm-2) when compared with controls (84±8mN.mm-2). Recovery from fatigue was improved in fatty and diabetic fatty groups compared with controls. Ventilator-induced diaphragmatic dysfunction was observed in each group, but AF remained higher in fatty (82±8mN.mm-2,P = 0.03) compared with controls (70±8mN.mm-2). There was neutral lipid droplet accumulation in fatty and diabetic fatty. There were shifts towards a higher cross-sectional-area (CSA) of myosin heavy chain isoforms (MyHC)-2A fibers in fatty and diabetic fatty compared with control rats (P = 0.002 and P<0.001, respectively) and a smaller CSA of MyHC-2X in fatty compared with diabetic fatty and control rats (P<0.001 and P<0.001, respectively). The phosphorylated total-protein-kinase-B (pAKT)/AKT ratio was higher in fatty (182±58%,P = 0.03), but not in diabetic fatty when compared with controls and monocarboxylate-transporter-1 was higher in diabetic fatty (147±36%,P = 0.04), but not in fatty. CONCLUSIONS: Diaphragmatic force is increased in Zucker obese rats before and after mechanical ventilation, and is associated with activation of AKT pathway signaling and complex changes in morphology.
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Jong et al. (2017) studied Obesity and Type II Diabetes (Animal Model) (n=80). Obesity and diabetes (Zucker fatty and diabetic fatty rats) vs. Zucker lean (control) rats was evaluated on Diaphragm active-force (AF) at rest (p=0.02). Diaphragm active-force was significantly higher in fatty rats (96±7 mN.mm-2) compared with controls (84±8 mN.mm-2, P=0.02), but not in diabetic fatty rats (90±17 mN.mm-2).
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