Basal fuel homoeostasis in symptomatic human immunodeficiency virus infection

1991 ◽  
Vol 80 (4) ◽  
pp. 359-365 ◽  
Author(s):  
M. J. T. Hommes ◽  
J. A. Romijn ◽  
E. Endert ◽  
J. K. M. Eeftinck Schattenkerk ◽  
H. P. Sauerwein

1. In eight clinically stable symptomatic human-immunodeficiency-virus-infected patients and in seven healthy control subjects, glucose and fat metabolism were studied, using indirect calorimetry and primed continuous infusions of [3-3H]glucose and [14C]palmitate. 2. Studies were performed in the post-absorptive state (16 h of overnight fasting) and again after 22 h of overnight fasting. 3. In the post-absorptive state, net fat oxidation and triacylglycerol (‘triglyceride’) concentrations were significantly higher in the patients, but concentrations and turnover of free fatty acids were not significantly different between patients and control subjects. After 22 h of overnight fasting, free fatty acid turnover in the patients rose to significantly higher levels when compared with the control subjects. 4. Post-absorptive glucose oxidation, glucose turnover and glucose clearance did not differ between patients and control subjects. Although fasting induced a significantly greater decline in glucose turnover in the patients, plasma glucose concentrations decreased comparably in patients and control subjects. 5. No differences were found in plasma concentrations of insulin or of the counter-regulatory hormones between patients and control subjects. 6. It is concluded that the metabolic adaptation to short-term starvation in clinically stable human-immunodeficiency-virus-infected patients differs from that in healthy control subjects. Short-term starvation results in a significantly greater fall in glucose turnover, whereas fat metabolism is clearly stimulated. These alterations cannot be explained by differences in the concentrations of insulin or of the counter-regulatory hormones.

2017 ◽  
Vol 23 (7) ◽  
pp. 577-583 ◽  
Author(s):  
Beatrice Frajo-Apor ◽  
Georg Kemmler ◽  
Silvia Pardeller ◽  
Markus Huber ◽  
Christian Macina ◽  
...  

AbstractObjectives:Social cognitive deficits have been discussed to be endophenotypes for schizophrenia and other serious mental illnesses. The current study aimed to assess emotional intelligence (EI) in unaffected siblings of schizophrenia patients to investigate its potential role as endophenotype for schizophrenia.Methods:EI was measured in 56 schizophrenia patients, 57 unaffected siblings, and 127 healthy control subjects by using the Mayer-Salovey-Caruso Emotional Intelligence Test (MSCEIT). In addition, non-social cognition was assessed with the Brief Assessment of Cognition in Schizophrenia (BACS). Linear mixed models with compound symmetric correlation structure were used for of the three groups with respect to EI and non-social cognition.Results:Schizophrenia patients showed significantly lower overall EI and performed significantly worse in three out of four MSCEIT branches compared to unaffected siblings and control subjects, whereas the two latter groups had comparable EI levels. Similar performance patterns (patients<unaffected siblings=control subjects) were found with respect to non-social cognition. Solely in the “Tower of London” test, siblings achieved significantly lower task scores compared to control subjects.Conclusions:Based on our results, EI as measured with the MSCEIT does not seem to represent a marker of risk for schizophrenia. Further investigations should concentrate on other EI measures to reassess this finding. (JINS, 2017,23, 577–583)


PEDIATRICS ◽  
1987 ◽  
Vol 79 (1) ◽  
pp. 157-160
Author(s):  
MARGARET C. FISHER

Relatively few pediatricians will ever care for a child with the acquired immunodeficiency syndrome (AIDS); yet, all will be asked questions about this disease. Parents want to know the risk of their children acquiring AIDS. The fear and even panic surrounding AIDS continues to escalate. To educate our patients and control panic, we must understand the disease and the routes of transmission. It is now clear that AIDS is one end of the spectrum of illness caused by the human immunodeficiency virus (HIV, formerly called HTLV-III/LAV). The virus is present in blood and body fluids. It is transmitted from person to person by sexual contact and by exchange of blood.


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