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pubmed: 0021-972X

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Hemoglobin Glycation Index Is Associated with Cardiovascular Diseases in People with Impaired Glucose Metabolism.
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Hemoglobin Glycation Index Is Associated with Cardiovascular Diseases in People with Impaired Glucose Metabolism.

J Clin Endocrinol Metab. 2017 May 23;:

Authors: Ahn CH, Min SH, Lee DW, Oh TJ, Kim KM, Moon JH, Choi SH, Park KS, Jang HC, Ha J, Sherman A, Lim S

Context: There is a substantial interindividual variation in the association between glycated hemoglobin (HbA1c) and plasma glucose concentrations. Its impact on cardiovascular disease (CVD) has not been comprehensively evaluated.
Objective: We examined associations between interindividual variations in HbA1c, which was estimated as the hemoglobin glycation index (HGI), and CVD.
Design, Setting, and Participants: We performed a cross-sectional analysis with 1248 treatment-naïve subjects with prediabetes or diabetes. The HGI was defined as the measured HbA1c minus predicted HbA1c which was calculated from the linear relationship between HbA1c and fasting plasma glucose levels.
Main outcome measures: The prevalence of composite and individual CVDs including coronary artery disease (CAD), stroke, and peripheral artery disease (PAD).
Results: The overall prevalence of composite CVD, and individual prevalence of CAD, stroke, and PAD were 10.3%, and 5.7%, 5.1%, and 1.3%, respectively. All these prevalences significantly increased from 1st to 3rd tertile of HGI. In multivariate analysis, the highest HGI tertile was independently associated with composite CVD (odds ratio [95% confidence interval]: 2.81 [1.59-4.98]), and individual CAD (2.30 [1.12-4.73]), stroke (3.40 [1.50-7.73]), and PAD (6.37 [1.18-34.33]) after adjustment for other CVD risk factors including HbA1c levels. Two consecutive measurements of HGI obtained on different days showed good correlation (r = 0.651, P <0.001) and high concordance rate in the tertile classification (69.1%).
Conclusions: High HGI was independently associated with overall and individual CVDs. This result suggests that discrepancy between HbA1c and fasting glucose levels can reflect vascular health in subjects with impaired glucose metabolism.

PMID: 28541544 [PubMed - as supplied by publisher]

Constitutive activation of AKT2 in humans leads to hypoglycemia without fatty liver or metabolic dyslipidemia.
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Constitutive activation of AKT2 in humans leads to hypoglycemia without fatty liver or metabolic dyslipidemia.

J Clin Endocrinol Metab. 2017 May 23;:

Authors: Minic M, Rocha N, Harris J, Groeneveld MP, Leiter S, Wareham N, Sleigh A, De Lonlay P, Hussain K, O'Rahilly S, Semple RK

Context: The activating p.Glu17Lys mutation in AKT2, a kinase mediating many of insulin's metabolic actions, causes hypoinsulinemic hypoglycemia and left-sided hemihypertrophy. The wider metabolic profile and longer term natural history of the condition has not yet been reported.
Objective: To characterise the metabolic and cellular consequences of the AKT2 p.Glu17Lys mutation in two previously reported males at the age of 17 years.
Design/intervention: Body composition analysis using dual energy X ray absorptiometry, overnight profiling of plasma glucose, insulin and fatty acids, oral glucose tolerance testing, and magnetic resonance spectroscopy to determine hepatic triglyceride content were undertaken. Hepatic de novo lipogenesis was quantified using deuterium incorporation into palmitate. Signaling in dermal fibroblasts was studied ex vivo.
Results: Both patients had 37% adiposity. One developed hypoglycemia after 2 hours of overnight fasting with concomitant suppression of plasma fatty acids and ketones, while the other maintained euglycemia with an increase in free fatty acids. Blood glucose excursions after oral glucose were normal in both patients, albeit with low plasma insulin concentrations. In both patients plasma triglyceride concentration, hepatic triglyceride content and fasting hepatic de novo lipogenesis were normal. Dermal fibroblasts of one proband showed low level constitutive phosphorylation of AKT and some downstream substrates, but no increased cell proliferation rate.
Conclusions: The p.Glu17Lys mutation of AKT2 confers low level constitutive activity upon the kinase, and produces hypoglycemia with suppressed fatty acid release from adipose tissue, but not fatty liver, hypertriglyceridaemia nor elevated hepatic de novo lipogenesis. Hypoglycemia may spontaneously remit.

PMID: 28541532 [PubMed - as supplied by publisher]