Navegando por Palavras-chave "beta-cell function"

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    beta-Cell function in individuals carrying the mitochondrial tRNA Leu (UUR) mutation
    (Lippincott Williams & Wilkins, 2007-01-01) Salles, Joao Eduardo; Kasamatsu, Teresa S.; Dib, Sergio A.; Moises, Regina S.; Universidade Federal de São Paulo (UNIFESP)
    Objectives: To assess the beta-cell function in individuals with mitochondrial DNA A3243G mutation with normal glucose tolerance (NGT) or diabetes mellitus (DM). Furthermore, in diabetic individuals, we evaluated the effect of coenzyme Q10 supplementation on insulin secretory response.Methods: Eight mutation-positive individuals with NGT (n = 4) or DM (n = 4) were studied. beta-Cell function was evaluated by C-peptide levels before and after a mixed liquid meal (Sustacal) challenge and by first-phase insulin response.Results: Fasting and Sustacal-stimulated C-peptide levels were significantly lower in diabetic patients than that in controls (area under the curve: 104.1 +/- 75.7 vs 520.8 +/- 173.8, P = 0.001), whereas in individuals with NGT, this response was preserved (area under the curve: 537.8 +/- 74.3 vs 520.8 +/- 179.8, P = 0.87). the duration of diabetes was negatively correlated with fasting C-peptide levels (r = -0.961, P = 0.038). Among the 3 patients with residual insulin secretion, the short-term treatment with coenzyme Q10 (3 months) improved C-peptide levels in 2 of them. the first-phase insulin response was diminished in 2 individuals with NGT, the oldest ones.Conclusions: We showed an impaired insulin secretory capacity in individuals carrying the A3243G mutation, this possibly being the primary defect contributing to the development of DM. in addition, our data suggest that this could be a functional defect.
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    Evidence for impaired insulin production and higher sensitivity in stunted children living in slums
    (Cambridge Univ Press, 2006-05-01) Martins, Paula Andrea [UNIFESP]; Sawaya, Ana Lydia [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The objective of the present study was to investigate the changes in glucose and insulin metabolism in nutritionally stunted children that can be involved in the appearance of chronic diseases in adulthood. for this purpose, sixty-one children were selected, thirty-five boys and twenty-six girls, residents of slums in São Paulo, Brazil. the children were classified according to the height-for-age as stunted (l-1.5 Z-score; n 21) or non-stunted (>-1.5 Z-score; n 40). the glucose and insulin plasma levels were determined and, from these values, the indexes that evaluate the pancreatic beta-cell function (homeostasis model assessment (HOMA-B)) and insulin sensitivity (HOMA-S) were assessed. Stunted children showed lower values of fasting insulin than those of the non-stunted group (boys: 29.7 (sd 14.9) v. 50.4 (sd 29.2) pmol/l, P=0.019; girls: 34.4 (sd 12.6) v. 62.3 (sd 28.7) pmol/l, P=0.016) but the glucose levels were similar (boys: 4.6 (sd 0.3) v. 4.5 (sd 0.3) mmol/l; girls: 4.2 (sd 0.3) v. 4.4 (sd 0.3) mmol/l). Stunted children showed lower HOMA-B values (boys: 83 (sd 22) % v. 115 (sd 36) %, P=0.011; girls: 107 (sd 23) % v. 144 (sd 46) %, P=0.045) and higher HOMA-S values (boys: 196 (sd 92) % v. 120 (sd 62) %, P=0.014; girls: 159 (sd 67) % v. 98 (sd 57) %, P=0.016). the results show a decreased activity of beta-cell function and increased insulin sensitivity in stunted children. the decreased beta-cell function of this group may strongly predict type 2 diabetes.
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    Prevalence of pancreatic autoantibodies in non-diabetic patients with autoimmune thyroid disease and its relation to insulin secretion and glucose tolerance
    (Sbem-Soc Brasil Endocrinologia & Metabologia, 2017) Sallorenzo, Carolina [UNIFESP]; Silva, Regina [UNIFESP]; Kasamatsu, Teresa [UNIFESP]; Dib, Sergio [UNIFESP]
    Objective: We evaluated the prevalence of glutamic acid decarboxylase (GADA) and tyrosine phosphatase-protein antibodies (IA2A), their titers and their relation to first phase insulin response (FPIR) and glucose tolerance in autoimmune thyroid diseases (ATDs) patients. Subjects and methods: Graves' disease (GD