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Insulin and muscle metabolism—Part I
440
Burns Vol. ~/NO. 6
unchanged in lung tissue and transiently increased in non-burned tissue. Lymph prostacyclin levels were increased 5 times in lung and 3.5 times in non-burned tissues. These levels returned to baseline at the same rate as the lymph flow. Thromboxane levels were not increased in lung, burned or non-burned tissue. In burned tissue the lymph flow increased between 5- and IO-fold as did protein permeability and the prostacyclin levels increased 36-fold. These increases persisted for at least 48 hours after injury. Harms 9. A., Bodai 9. I., Smith M. et al. (198 I) Prostaglandin release and altered microvascular integrity aher burn injury. J. Surg. Res. 31, 274.
latory effect of insulin was completely absent in soleus muscle from the burned limb. All these observations suggest at burning injury suppresses the insulin-induced augmentation of glucose uptake and glucose incorporation into glycogen in skeletal muscles in the region of the burn but does not alter insulin sensitivity of skeletal muscles in the unburned region. Nelson K. M. and Turinsky J. (198 I) Local effect of burn on skeletal muscle insulin responsiveness. J. Surg. Res. 31,288.
Insulin and muscle metabolism-Part
Insulin and muscle metabolism-Part
I
Basal and insulin-stimulated glucose metabolism by skeletal muscle were studied for 3 days after a scald to one hind limb of a rat. Soleus muscles from the burned and unburned limb of the burned rats as well as from control animals were incubated with radioactive glucose and various quantities of insulin. Basal glucose uptake by soleus muscle from the burned limb was 1.44 times greater than that of the controls. Glucose uptake by muscle from the unburned limb did not differ from that of controls. Insulin increased glucose uptake in control and unburned muscles but had no effect in burned muscles. Basal lactic acid release by soleus muscle from the burned limb and the contralateral unburned limb of burned rats was 123 per cent and 24 per cent higher respectively than that of soleus muscle from control rats. Of the lactic acid released by muscles from control rats or the unburned limb of burned rats, 35 per cent was derived from exogenous glucose, whereas 50-55 per cent of the lactic acid released by muscles from the burned limb was derived from exogenous glucose, reflecting a predominant conversion ofglucose to lactic acid. Insulin had no effect on the rate of lactic acid release and did not change the proportion of glucose converted to lactic acid by any of the muscle groups. The basal rate of glucose conversion to CO, by muscle from the burned-limb was increased (I 33 per cent), whereas that bv muscle from the unburned limb was not altered as compared to controls. Insulin did not stimulate the conversion of glucose to CO, by any of the muscle groups, and in the presence of insulin the release of CO, bv burned, unburned and control muscle did not differ. The basal rate of glucose incorporation into glycogen was the same in all three muscle groups. Insulin stimulated glucose incorporation into glycogen to a similar extent in muscles from control rats and the unburned limb of burned rats. However the stimu-
II
Three days after scalding one hind limb of a rat, soleus muscle from the burned limb, but not from the contralateral unburned limb, failed to increase its rate of glucose incorporation into glycogen in response to in vitro stimulation with insulin. This lack ofresponse to insulin is not due to the release by burned muscle of a substance that would either degrade insulin or decrease its biological potency. The insulin resistance is also not related to morphological changes in muscle because it is shown both by the portion of muscle that shows inflammatory and degenerative changes, and the portion of muscle that is electron microscopically indistinguishable from normal tissue. The insulin unresponsiveness cannot be reversed by addition of the ATP/Mg Cl, complex. The binding of insulin to its receptors in the intact soleus muscle from the burned limb does not differ from controls at low insulin concentrations (0.1-1.0 mu) and is only one third lower (at IO mU per ml). This change in the capacity of burned muscle to bind insulin is not of sufficient magnitude to account for the complete lack of response to the hormone. Since in the absence of insulin, soleus muscle from the burned limb can convert glucose to glycogen and can respond to increased substrate availability by augmenting glycogen synthesis, the failure of muscle underlying the burn wound to respond to insulin appears to be due to a defect in coupling of the insulin receptor with intracellular effecters and/or in a component of the complex enzymatic machinery regulating glycogen metabolism. Nelson K. M. and Turinsky J. (1981) Analysis of post-burn insulin unresponsiveness in skeletal muscle. J. Surg. Rex 31,404.
References and abstracts compiled by J. W. L. Davies DSc, Department of Surgery, Glasgow Royal Infirmary, using Current Contents and the British Library Automated Information Services supplied to Wakefield Postgraduate Medical Centre, West Yorkshire.
Burns Vol. ~/NO. 6
unchanged in lung tissue and transiently increased in non-burned tissue. Lymph prostacyclin levels were increased 5 times in lung and 3.5 times in non-burned tissues. These levels returned to baseline at the same rate as the lymph flow. Thromboxane levels were not increased in lung, burned or non-burned tissue. In burned tissue the lymph flow increased between 5- and IO-fold as did protein permeability and the prostacyclin levels increased 36-fold. These increases persisted for at least 48 hours after injury. Harms 9. A., Bodai 9. I., Smith M. et al. (198 I) Prostaglandin release and altered microvascular integrity aher burn injury. J. Surg. Res. 31, 274.
latory effect of insulin was completely absent in soleus muscle from the burned limb. All these observations suggest at burning injury suppresses the insulin-induced augmentation of glucose uptake and glucose incorporation into glycogen in skeletal muscles in the region of the burn but does not alter insulin sensitivity of skeletal muscles in the unburned region. Nelson K. M. and Turinsky J. (198 I) Local effect of burn on skeletal muscle insulin responsiveness. J. Surg. Res. 31,288.
Insulin and muscle metabolism-Part
Insulin and muscle metabolism-Part
I
Basal and insulin-stimulated glucose metabolism by skeletal muscle were studied for 3 days after a scald to one hind limb of a rat. Soleus muscles from the burned and unburned limb of the burned rats as well as from control animals were incubated with radioactive glucose and various quantities of insulin. Basal glucose uptake by soleus muscle from the burned limb was 1.44 times greater than that of the controls. Glucose uptake by muscle from the unburned limb did not differ from that of controls. Insulin increased glucose uptake in control and unburned muscles but had no effect in burned muscles. Basal lactic acid release by soleus muscle from the burned limb and the contralateral unburned limb of burned rats was 123 per cent and 24 per cent higher respectively than that of soleus muscle from control rats. Of the lactic acid released by muscles from control rats or the unburned limb of burned rats, 35 per cent was derived from exogenous glucose, whereas 50-55 per cent of the lactic acid released by muscles from the burned limb was derived from exogenous glucose, reflecting a predominant conversion ofglucose to lactic acid. Insulin had no effect on the rate of lactic acid release and did not change the proportion of glucose converted to lactic acid by any of the muscle groups. The basal rate of glucose conversion to CO, by muscle from the burned-limb was increased (I 33 per cent), whereas that bv muscle from the unburned limb was not altered as compared to controls. Insulin did not stimulate the conversion of glucose to CO, by any of the muscle groups, and in the presence of insulin the release of CO, bv burned, unburned and control muscle did not differ. The basal rate of glucose incorporation into glycogen was the same in all three muscle groups. Insulin stimulated glucose incorporation into glycogen to a similar extent in muscles from control rats and the unburned limb of burned rats. However the stimu-
II
Three days after scalding one hind limb of a rat, soleus muscle from the burned limb, but not from the contralateral unburned limb, failed to increase its rate of glucose incorporation into glycogen in response to in vitro stimulation with insulin. This lack ofresponse to insulin is not due to the release by burned muscle of a substance that would either degrade insulin or decrease its biological potency. The insulin resistance is also not related to morphological changes in muscle because it is shown both by the portion of muscle that shows inflammatory and degenerative changes, and the portion of muscle that is electron microscopically indistinguishable from normal tissue. The insulin unresponsiveness cannot be reversed by addition of the ATP/Mg Cl, complex. The binding of insulin to its receptors in the intact soleus muscle from the burned limb does not differ from controls at low insulin concentrations (0.1-1.0 mu) and is only one third lower (at IO mU per ml). This change in the capacity of burned muscle to bind insulin is not of sufficient magnitude to account for the complete lack of response to the hormone. Since in the absence of insulin, soleus muscle from the burned limb can convert glucose to glycogen and can respond to increased substrate availability by augmenting glycogen synthesis, the failure of muscle underlying the burn wound to respond to insulin appears to be due to a defect in coupling of the insulin receptor with intracellular effecters and/or in a component of the complex enzymatic machinery regulating glycogen metabolism. Nelson K. M. and Turinsky J. (1981) Analysis of post-burn insulin unresponsiveness in skeletal muscle. J. Surg. Rex 31,404.
References and abstracts compiled by J. W. L. Davies DSc, Department of Surgery, Glasgow Royal Infirmary, using Current Contents and the British Library Automated Information Services supplied to Wakefield Postgraduate Medical Centre, West Yorkshire.