Introduction: Whether menopause increases the risk of type 2 diabetes mellitus (T2DM) independently of ageing has been a matter of debate. Controversy also exists about the benefits and risks of menopausal hormone therapy (MHT) in women with T2DM. Aims: To summarise the evidence on 1) the effect of menopause on metabolic parameters and the risk of T2DM, 2) the effect of T2DM on age at menopause, 3) the effect of MHT on the risk of T2DM, and 4) the management of postmenopausal women with T2DM. Materials and methods: Literature review and consensus of experts' opinions. Results and conclusion: Metabolic changes during the menopausal transition include an increase in and the central redistribution of adipose tissue, as well as a decrease in energy expenditure. In addition, there is impairment of insulin secretion and insulin sensitivity and an increase in the risk of T2DM. MHT has a favourable effect on glucose metabolism, both in women with and in women without T2DM, while it may delay the onset of T2DM. MHT in women with T2DM should be administered according to their risk of cardiovascular disease (CVD). In women with T2DM and low CVD risk, oral oestrogens may be preferred, while transdermal 17βoestradiol is preferred for women with T2DM and coexistent CVD risk factors, such as obesity. In any case, a progestogen with neutral effects on glucose metabolism should be used, such as progesterone, dydrogesterone or transdermal norethisterone. Postmenopausal women with T2DM should be managed primarily with lifestyle intervention, including diet and exercise. Most of them will eventually require pharmacological therapy. The

IntroductIon The degeneration of retinal neurons and glial cells has recently been postulated in the pathogenesis of diabetic retinopathy. Optical coherence tomography (OCT) allows to perform qualitative and quantitative measurements of retinal thickness (RT) with identification of individual retinal layers. objectIves We compared RT, retinal nerve fiber layer (RNFL) thickness, and ganglion cell layer (GCL) thickness obtained by OCT in type 1 diabetic patients with and without clinically diagnosed retinopathy. PAtIents And methods The study included 77 consecutive patients with type 1 diabetes (39 men, 38 women; median age, 35 years [interquartile range (IQR), 29-42]; median disease duration, 10 years [IQR, 9-14]) and 31 age-and sex-matched controls. We measured RT in the fovea, parafovea, and perifovea, as well as RNFL and GCL thickness. We divided diabetic patients into 2 subgroups, i.e., those with diabetic retinopathy and without retinopathy. results We observed thicker perifoveal retina (P = 0.05), mean RNFL (P = 0.002), inferior RNFL (P <0.0001), and superior and inferior GCL (P = 0.05 and P = 0.04, respectively) in diabetic subjects compared with the control group. We detected retinopathy in 23 diabetic patients (29%). Compared with patients without retinopathy, subjects with retinopathy had thinner parafoveal retina (P = 0.05), mean RNFL (P = 0.002), inferior and nasal RNFL (P = 0.002, P = 0.03), superior (P = 0.05) and inferior GCL (P = 0.006). Significant correlations were found between duration of diabetes and nasal RNFL thickness (r =-0.32, P = 0.004) and parafoveal RT (r =-0.47, P <0.001). conclusIons The results might suggest the loss of intraretinal neural tissue in type 1 diabetic patients with retinopathy. Neurodegeneration in diabetic retinopathy is closly associated with disease duration.

AimsTo assess the prevalence of ZnT8-ab and its correlation to other autoimmune markers and diabetic ketoacidosis occurrence in children and adults with T1DM onset. MethodsThe study included 367 patients (218 children; 149 adults) at the T1DM onset. Selected diabetes-related autoantibodies such as GAD-ab, IA2-ab, ZnT8-ab were tested before the initiation of insulin therapy. Diabetic ketoacidosis was defined as glucose concentration > 13.9 mmol/l, pH < 7.30, concentration of HCO3 < 15 mmol/l, presence of ketone bodies in the blood and urine.ResultsThe autoantibodies pattern differs in both study groups. Children were mostly positive for two (37.8%) and three (49.5%) autoantibodies, whereas adults for one (32.2%) and two (30.7%). The most frequently detected autoantibodies in youth were ZnT8-ab (81.1%) and IA2-ab (80.7%), while in adults GAD-ab (74.8%). ZnT8-ab (p < 0.0001) titers were significantly higher in children, but adults had higher titer of GAD-ab (p < 0.0001) and IA2-ab (p < 0.0001). Children developed more frequently diabetic ketoacidosis (28.4 vs. 10.7%, p = 0.0002). ZnT8-ab (p = 0.002) and IA2-ab (p = 0.008) were reported mostly in individuals with ketoacidosis. A correlation between the number of positive antibodies and the severity of ketoacidosis was observed (Rs − 0.129 p = 0.014). ZnT8-ab were associated with a greater risk of ketoacidosis independent of gender, age group and the autoantibodies number [OR = 2.44 (95% CI 1.0–5.94), p = 0.04]. ConclusionsChildren are at greater risk of ketoacidosis at the diagnosis of diabetes. ZnT8-ab and IA2-ab are commonly detected in children, while adults have frequently higher titer of GAD-ab. ZnT8-ab are associated with more acute diabetes onset.Electronic supplementary materialThe online version of this article (10.1007/s00592-017-1091-x) contains supplementary material, which is available to authorized users.

We have shown that the presence of retinopathy in type 1 diabetic patients is associated with subclinical atherosclerosis and wave reflection.

Changes in sensitivity to insulin occur in the course of a number of endocrine disorders. Most of the hormones through their antagonistic action to insulin lead to increased hepatic glucose output and its decreased utilisation in peripheral tissues. Carbohydrate disorders observed in endocrine diseases result from the phenomenon of insulin resistance, and in some cases also a reduction in insulin secretion is present. Abnormalities of glucose metabolism are observed in acromegaly, but also in growth hormone deficiency, hypercortisolism in the course of Cushing's syndrome, hyper- or hypothyroidism, primary hyperparathyroidism, aldosteronism, pheochromocytoma, congenital hypertrophy of the adrenal glands, polycystic ovaries syndrome, hypogonadism, or other hormonally active neuroendocrine tumours. They are of a secondary nature in relation to impaired hormonal balance. Hyperglycaemia is therefore often reversible, and the most effective method of treatment of impaired insulin sensitivity is successful therapy of specific endocrinopathies. Insulin sensitisers, also with a good effect, are used. Most experiences to date can be attributed to metformin therapy. Attempts have been made at treatment with other agents that are also effective in reducing insulin resistance as incretins or glitazones. In the presented paper, the authors reviewed endocrine diseases in which there is a clinically significant change in insulin sensitivity. Moreover, methods of therapy of concomitant disturbed glucose metabolism were presented.