Irregular Plasma Glucose Concentrations, Elevated Plasma Non-estcrified Fatty Acid Concentrations and Unchanged Glucokinase Activities in Brain, Muscle and Liver during Pregnancy Toxaemia in Sheep

1966 ◽  
Vol 7 (4) ◽  
pp. 493-498 ◽  
Author(s):  
D.S. Kronfeld ◽  
Fiora Raggi
1986 ◽  
Vol 251 (6) ◽  
pp. E703-E706 ◽  
Author(s):  
C. C. Coimbra ◽  
R. H. Migliorini

Previous studies indicated that a longitudinal pathway connecting preoptic, lateral, and posterior hypothalamic areas participates in the process of free fatty acid (FFA) mobilization in the rat. In the present experiments, the presence of sensitive neurons in the preoptic area was investigated by examining the effects of topical stimulation with 2-deoxyglucose (2-DG) or insulin on the levels of plasma FFA in conscious unrestrained rats. Microinjections of minute amounts (50 micrograms and 1 microliter) of 2-DG into the preoptic area of fed animals induced rapid increases in the concentration of plasma FFA. Microinjections of insulin (5 microU and 0.5 microliter) produced sharp decreases of the elevated plasma FFA levels in fasted rats. Both 2-DG and insulin induced small increases in plasma glucose that did not differ from similar increases induced by equal volumes of 0.15 M NaCl. The results provide direct evidence for the presence within the preoptic area of insulin-sensitive glucoreceptors involved in FFA mobilization. The data suggest that activation of these receptors and increased sympathetic outflow to adipose tissue contributes to fasting lipolysis.


Diabetes Care ◽  
1989 ◽  
Vol 12 (4) ◽  
pp. 276-281 ◽  
Author(s):  
K. E. Friday ◽  
M. T. Childs ◽  
C. H. Tsunehara ◽  
W. Y. Fujimoto ◽  
E. L. Bierman ◽  
...  

Diabetes ◽  
1988 ◽  
Vol 37 (8) ◽  
pp. 1020-1024 ◽  
Author(s):  
G. M. Reaven ◽  
C. Hollenbeck ◽  
C. Y. Jeng ◽  
M. S. Wu ◽  
Y. D. Chen

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 5364-5372 ◽  
Author(s):  
Eric D. Bruder ◽  
Ping C. Lee ◽  
Hershel Raff

Abstract Neonatal hypoxia is a common condition resulting from pulmonary and/or cardiac dysfunction. Dexamethasone therapy is a common treatment for many causes of neonatal distress, including hypoxia. The present study examined the effects of dexamethasone treatment on both normoxic and hypoxic neonatal rats. We performed comprehensive hepatic fatty acid/lipid profiling and evaluated changes in pertinent plasma hormones and lipids and a functional hepatic correlate, i.e. hepatic lipase activity. Rats were exposed to hypoxia from birth to 7 d of age. A 4-d tapering dose regimen of dexamethasone was administered on: postnatal day (PD)3 (0.5 mg/kg), PD4 (0.25 mg/kg), PD5 (0.125 mg/kg), and PD6 (0.05 mg/kg). The most significant finding was that dexamethasone attenuated nearly all hypoxia-induced changes in hepatic lipid profiles. Hypoxia increased the concentration of hepatic triacylglyceride and free fatty acids and, more specifically, increased a number of fatty acid metabolites within these lipid classes. Administration of dexamethasone blocked these increases. Hypoxia alone increased the plasma concentration of cholesterol and triacylglyceride, had no effect on plasma glucose, and only tended to increase plasma insulin. Dexamethasone administration to hypoxic pups resulted in an additional increase in plasma lipid concentrations, an increase in insulin, and a decrease in plasma glucose. Hypoxia and dexamethasone treatment each decreased total hepatic lipase activity. Normoxic pups treated with dexamethasone displayed increased plasma lipids and insulin. The effects of dexamethasone on hepatic function in the hypoxic neonate are dramatic and have significant implications in the assessment and treatment of metabolic dysfunction in the newborn.


1971 ◽  
Vol 49 (5) ◽  
pp. 394-398 ◽  
Author(s):  
W. D. Wagner ◽  
R. A. Peterson ◽  
R. J. Cenedella

Plasma free fatty acid (FFA) levels and the effects of prostaglandin E1 (PGE1) were studied in cold-acclimated and cold-exposed chickens and compared to controls. Chickens cold-acclimated at 4–7 or 8–11 °C for 4 weeks had significantly elevated plasma FFA when compared to the controls at 19–21 °C. Although PGE1 had no effect on the basal level of FFA of controls, a significantly lower plasma FFA was seen after injection of either 10 or 30 μg PGE1/kg in cold-acclimated chickens. Chickens cold-exposed to 2–3 °C for 4 h demonstrated significant elevations of plasma FFA when compared to controls. Only 30 μg PGE1/kg significantly depressed the plasma FFA in the cold-exposed birds. No inhibition of basal FFA release was seen in control animals. From these experiments, it is concluded that chickens mobilize FFA extensively under cold-exposure and that this stimulated lipolysis is inhibited by PGE1.


1997 ◽  
Vol 273 (3) ◽  
pp. E644 ◽  
Author(s):  
R E Pratley ◽  
M Nicolson ◽  
C Bogardus ◽  
E Ravussin

Leptin is believed to play a role in the regulation of energy balance, but little is known about factors influencing plasma leptin concentrations. To determine the effect of short-term changes in energy balance, we measured plasma leptin concentrations as well as plasma glucose, insulin, triglyceride, nonesterified fatty acid concentrations, and metabolic rate in response to a standard test meal followed by a 24-h fast in 21 healthy Pima Indians. Plasma leptin concentrations decreased by 8% (P < 0.05) 2-4 h after the test meal. They returned to baseline 6-12 h after the subjects ate, then subsequently decreased, and, by the end of the fast, were an average of 37% below baseline (P < 0.0001). Changes in plasma leptin concentrations did not correlate with changes in plasma glucose, insulin, triglyceride, or nonesterified fatty acid concentrations or with changes in metabolic rate. The results of this study indicate that plasma leptin concentrations decrease in response to short-term energy restriction. These changes were not due to changes in glucose, insulin, triglycerides, or nonesterified fatty acids, nor did they relate to changes in metabolic rate. The decrease in plasma leptin concentrations with fasting may be an important homeostatic response to an energy deficit, stimulating food intake and thus restoring energy balance.


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