scholarly journals Metabolic changes in rats during developing thiamin deficiency.(Short Communications)

1975 ◽  
Vol 146 (3) ◽  
pp. 739-740 ◽  
Author(s):  
C C Liang

Determinations of rectal temperature, blood glucose, plasma free fatty acids, liver acetyl-CoA and carcass fat of thiamin-deficient rats indicated that during the ensuing anorexia they metabolized their fat reserves more rapidly than did pair-fed normal controls. Their lower metabolic rate indicates that the reserves mobilized are utilized inefficiently.

1988 ◽  
Vol 255 (4) ◽  
pp. R547-R556 ◽  
Author(s):  
A. J. Scheurink ◽  
A. B. Steffens ◽  
L. Benthem

The effects of intravenously and intrahypothalamically administered alpha- and beta-adrenoceptor antagonists on exercise-induced alterations in blood glucose, plasma free fatty acids (FFA), and insulin were investigated in rats. Exercise consisted of strenuous swimming against a counter current for 15 min. Before, during, and after swimming, blood samples were withdrawn through a permanent heart catheter. Intravenous administration of the alpha-blocker phentolamine led to a reduction in glucose and a substantial increase in insulin levels. Infusion of phentolamine through permanent bilateral cannulas into either the ventromedial or lateral area of the hypothalamus (VMH and LHA, respectively) completely prevented the increase in glucose while the decline in insulin was unaffected. Infusion of phentolamine into the VMH caused much higher plasma FFA levels than in controls. The beta-blocker timolol given intravenously caused a delayed increase in glucose and prevented the increase in FFA. Infusion of timolol into either VMH or LHA caused a delay in the increase in both glucose and FFA. The results suggest that 1) both peripheral and hypothalamic adrenoceptors are involved in energy metabolism during exercise and 2) FFA, glucose, and insulin concentrations in blood are independently regulated by VMH and LHA.


1971 ◽  
Vol 118 (545) ◽  
pp. 429-436 ◽  
Author(s):  
Werner H. Schimmelbusch ◽  
Peter S. Mueller ◽  
Jack Sheps

Various abnormalities have been demonstrated in schizophrenic patients in response to injected insulin. Thomaset al.(22), Harris (8), Freemanet al.(7), Mayer-Gross (10), and Bracelandet al.(4) have shown a delayed or decreased response of blood glucose to insulin in schizophrenic patients. Meduna and McCulloch (11) observed that those schizophrenic patients who suffered from confusion and clouding of the sensorium particularly displayed a delayed or decreased response to injected insulin as well as a urinary hyperglycaemic factor and decreased tolerance to oral and intravenous glucose. Subsequent studies by Mueller (12, 13) demonstrated a rise or lack of fall in the plasma free fatty acids (FFA) following the administration of insulin intramuscularly or intravenously in chronic schizophrenic patients. Van Sickleet al.(23) confirmed these findings of insulin resistance in chronic schizophrenia and noted that this low FFA response was neither related to an abnormal release of, nor response to, epinephrine.


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