Glucose-insulin metabolism in chronic schizophrenia

Author(s):  
F. Brambilla ◽  
A. Guastalla ◽  
A. Guerrini ◽  
F. Riggi ◽  
C. Rovere ◽  
...  
2007 ◽  
Vol 1 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Eric Pihlgren ◽  
Nash Boutros

2012 ◽  
Vol 5 (4) ◽  
pp. 185-192 ◽  
Author(s):  
J. Lindenmayer ◽  
Frank Tedeschi ◽  
Anna Yusim ◽  
Anzalee Khan ◽  
Saurabh Kaushik ◽  
...  

1986 ◽  
Vol 111 (4) ◽  
pp. 516-521
Author(s):  
Nina Clausen ◽  
Per-Eric Lins ◽  
Ulf Adamson ◽  
Bertil Hamberger ◽  
Suad Efendić

Abstract. Hypothyroidism has been alleged to modulate insulin action and influence the secretion of growth hormone and catecholamines. We recently investigated the influence of hypothyroidism on glucose counterregulatory capacity and the hormonal responses to insulin-induced hypoglycaemia in 6 patients with primary hypothyroidism (age 32–52 years, TSH-values 66–200 mU/l). Hypoglycaemia was induced in the hypothyroid state and again when the subjects were euthyroid. After an overnight fast a constant rate infusion of insulin (2.4 U/h) was given for 4 h. Glucose was measured every 15 min and insulin, C-peptide, glucagon, epinephrine, norepinephrine, growth hormone and cortisol every 30 min for 5 h. During insulin infusion somewhat higher concentrations of the hormone were obtained in the hypothyroid state and simultaneously glucose levels were 0.5 mmol/l lower. As expected, basal norepinephrine levels were higher in hypothyroidism. However, no increase in circulating norepinephrine during hypoglycaemia was registered in the two experiments. The responses of counterregulatory hormones showed an enhanced response of cortisol, similar responses of growth hormone and epinephrine while the glucagon response was paradoxically impaired. Our findings suggest that hypothyroidism alters insulin metabolism, and that the glucagon response to hypoglycaemia is impaired in this condition.


2004 ◽  
Vol 34 (3) ◽  
pp. 401-412 ◽  
Author(s):  
R. McCABE ◽  
I. LEUDAR ◽  
C. ANTAKI

Background. Having a ‘theory of mind’ (ToM) means that one appreciates one's own and others' mental states, and that this appreciation guides interactions with others. It has been proposed that ToM is impaired in schizophrenia and experimental studies show that patients with schizophrenia have problems with ToM, particularly during acute episodes. The model predicts that communicative problems will result from ToM deficits.Method. We analysed 35 encounters (>80 h of recordings) between mental health professionals and people with chronic schizophrenia (out-patient consultations and cognitive behaviour therapy sessions) using conversation analysis in order to identify how the participants used or failed to use ToM relevant skills in social interaction.Results. Schizophrenics with ongoing positive and negative symptoms appropriately reported first and second order mental states of others and designed their contributions to conversations on the basis of what they thought their communicative partners knew and intended. Patients recognized that others do not share their delusions and attempted to reconcile others' beliefs with their own but problems arose when they try to warrant their delusional claims. They did not make the justification for their claim understandable for their interlocutor. Nevertheless, they did not fail to recognize that the justification for their claim is unconvincing. However, the ensuing disagreement did not lead them to modify their beliefs.Conclusions. Individuals with schizophrenia demonstrated intact ToM skills in conversational interactions. Psychotic beliefs persisted despite the realization they are not shared but not because patients cannot reflect on them and compare them with what others believe.


Metabolites ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 34
Author(s):  
Irina A. Mednova ◽  
Alexander A. Chernonosov ◽  
Marat F. Kasakin ◽  
Elena G. Kornetova ◽  
Arkadiy V. Semke ◽  
...  

Amino acids and acylcarnitines play an important role as substrates and intermediate products in most of pathways involved in schizophrenia development such as mitochondrial dysfunction, inflammation, lipid oxidation, DNA damage, oxidative stress, and apoptosis. It seems relevant to use an integrated approach with ‘omics’ technology to study their contribution. The aim of our study was to investigate serum amino acid and acylcarnitine levels in antipsychotics-treated patients with chronic schizophrenia compared with healthy donors. We measured serum levels of 15 amino acids and 30 acylcarnitines in 37 patients with schizophrenia and 36 healthy donors by means of tandem mass spectrometry. In summary, patients with chronic schizophrenia had an altered concentration of a few amino acids and acylcarnitines in comparison to the healthy probands. Further research is needed to assess and understand the identified changes.


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