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PubMedDate not supplied

[Effect of sulfonylurea preparations on the course of pregnancy and the state of the fetuses of female rats with alloxan prediabetes, latent diabetes and mild forms of manifest diabetes].

The influence of antidiabetic sulphanylamides, used before the occurrence of pregnancy, on the weight of fetuses and placentae was revealed in rats with alloxan "prediabetes", latent diabetes, and manifest diabetes. Diabetes compensation before the occurrence of pregnancy in rats with "prediabetes" and latent diabetes by means of chlorpropamide, and in rats with manifest diabetes with chlorpropamide together with biguanides led to a significant reduction of the weight of fetuses and prevented their death.

Animals↗
PubMed1989

Preclinical and manifest diabetes mellitus in young patients with Friedreich's ataxia: no evidence of immune process behind the islet cell destruction.

Friedreich's ataxia is known to be associated with diabetes mellitus in up to 20% of the patients. However, type, development and course of diabetes mellitus are not well characterised. We report on 3 patients (2 female and 1 male, age 13-20 years) with the combination of Friedreich's ataxia and diabetes mellitus. Diabetes mellitus was characterised as follows: (1) it was strictly insulin-dependent and ketosis-prone, (2) the average insulin requirement was 1 U/kg body weight, (3) the HLA haplotype was not typical of Type 1 (insulin-dependent) diabetes mellitus, (4) there were no positive immune parameters typical of Type 1 diabetes at the clinical onset of diabetes mellitus and (5) there was no remission. To evaluate a preclinical phase as in common autoimmune Type 1 diabetes, i.v. glucose tolerance tests (0.5 g glucose/kg body weight) were performed in 8 patients with Friedreich's ataxia without diabetes mellitus. Seven patients had normal early phase insulin response. In contrast, the glucose disappearance rate was slow in 4 and normal in 3 patients. One of the 8 patients showed a prediabetic metabolic state: the early-phase insulin response was abolished and the glucose disappearance rate was abnormal. The results suggest that diabetes in Friedreich's ataxia is caused by a loss of islet cells similar to common Type 1 diabetes but without HLA-association and without serologic evidence for autoimmune destruction of the islet cells.

Adolescent↗
PubMed2004

Acarbose slows progression of intima-media thickness of the carotid arteries in subjects with impaired glucose tolerance.

BACKGROUND AND PURPOSE: Impaired glucose tolerance (IGT)-a prediabetic state-is an important risk factor for atherosclerosis. Acarbose, an alpha-glucosidase inhibitor, was shown in the placebo-controlled prospective study to prevent noninsulin-dependent diabetes mellitus (STOP-NIDDM) trial to reduce the risk of diabetes by 36% in IGT subjects. This article reports on a placebo-controlled subgroup analysis of the STOP-NIDDM study to examine the efficacy of acarbose to slow progression of intima-media thickness (IMT) in subjects with IGT. METHODS: One hundred thirty-two IGT subjects were randomized to placebo (n=66) or acarbose (n=66) 100 mg 3 times daily; the study duration was at least 3 years, mean follow-up time 3.9 (SD 0.6) years. Carotid IMT was determined at study entry and the end of the trial. The intent-to-treat analysis included 56 subjects in the acarbose and 59 in the control group who had a baseline and endpoint measurement. RESULTS: A significant reduction of the progression of IMT(mean) was observed in the acarbose group versus placebo. After an average time of 3.9 years, IMT(mean) increased by 0.02 (0.07) mm in the acarbose group versus 0.05 (0.06) mm in the placebo group (P=0.027). The annual increase of IMT(mean) was reduced by approximately 50% in the acarbose group versus placebo. Multiple linear regression revealed IMT progression as significantly related to acarbose intake. CONCLUSIONS: Acarbose slows progression of IMT in IGT subjects, a high-risk population for diabetes and atherosclerosis. This is the first placebo-controlled prospective subgroup analysis, demonstrating that counterbalancing of postprandial hyperglycemia may be vasoprotective.

Acarbose↗
PubMed2026

Comparison of Traditional Chinese Exercise and Equipment-Based Exercise on Glycaemic Control and Vitamin D Levels in Middle-Aged and Elderly Patients With Prediabetes: A Randomised Controlled Trial.

BACKGROUND: Prediabetes is a critical window for preventing progression to type 2 diabetes mellitus (T2DM). Both vitamin D deficiency and physical inactivity are associated with impaired glucose metabolism. This study compared the effects of Traditional Chinese Exercise (TCE) and Kuanle Equipment Exercise (KEE) on glycaemic measures, lipid profiles, body composition and serum 25-hydroxyvitamin D3 [25(OH)D3] in middle-aged and elderly adults with prediabetes. METHODS: We conducted a 12-week, single-centre, randomised controlled trial involving 62 participants with prediabetes (mean age 55.2 ± 8.4 years; 88.7% female). Participants were randomly assigned to control (usual care, n = 21), TCE (n = 20), or KEE (n = 21). Primary outcomes included fasting plasma glucose (FPG), 2-h OGTT glucose, glycated haemoglobin (HbA1c) and serum 25(OH)D3. Secondary outcomes comprised triglycerides, total cholesterol, LDL-C, HDL-C and body composition. RESULTS: At baseline, mean serum 25(OH)D3 was 21.53 ± 3.90 nmol/L. At 12 weeks, both TCE and KEE improved FPG, 2-h OGTT glucose, HbA1c and 25(OH)D3 versus control (all p ≤ 0.001). Relative changes in FPG were -9.4% (TCE) and -15.2% (KEE) versus -1.5% (control); corresponding changes were -14.6% and -21.2% for 2-h OGTT glucose, -6.7% and -12.9% for HbA1c, and +60.6% and +81.9% for 25(OH)D3. Direct TCE-KEE comparisons were not significant (all p > 0.05). In an exploratory analysis, change in 25(OH)D3 was inversely associated with change in 2-h OGTT glucose (partial r = -0.358, p = 0.006), but not with FPG, HbA1c, or triglycerides. CONCLUSIONS: Both TCE and KEE improved glycaemic outcomes and increased serum 25(OH)D3 compared with usual care in middle-aged and elderly adults with prediabetes. Although KEE produced numerically larger estimates, direct between-group comparisons were not significant, and the superiority of KEE over TCE was not established. These vitamin D findings require confirmation in trials that quantify sunlight exposure and dietary vitamin D intake.

Aged↗
PubMed1996

Toward an integrated phenotype in pre-NIDDM.

The search for the genetic basis of NIDDM has magnified the need for an efficient representation of the pre-NIDDM phenotype. The overall goal is to relate specific mutations on the genome to specific changes in physiologic function which lead to NIDDM. Unfortunately, there is still not a clear understanding of the molecular cause of NIDDM in most individuals. Therefore, one must take an alternative approach: to express in quantitative terms the various tissue processes which determine the ability to regulate the blood glucose in fasting and after carbohydrate administration. A minimal list of such processes includes the provision of glucose by the liver, insulin sensitivity, insulin secretion, and glucose effectiveness. The latter function is the ability of glucose per se to enhance glucose disappearance from blood, independent of a dynamic insulin response. Approaches to measuring the list of functions which determine the glucose tolerance are reviewed: they include the minimal model method, which quantitates insulin sensitivity (Sl) and glucose effectiveness (SG), and a combined model approach, which measures insulin secretion. These methods are being developed for large populations. Such a development is important for elucidating the causes of reduced glucose tolerance in populations, and examining the relation between such causes and outcomes including diabetes and cardiovascular disease. Of particular importance for diabetes development is the characteristic hyperbolic relationship between insulin secretion and insulin action. This relationship, the "hyperbolic law of glucose tolerance' indicates that insulin secretion can only be assessed in terms of the ambient degree of insulin sensitivity. By applying this principle, it is clear that latent pancreatic islet-cell dysfunction has been underestimated, and may be significant even in subjects with impaired glucose tolerance. Finally, new explorations of insulin control of liver glucose output indicate that this process may be under the control of free fatty acids. The latter realization indicates that the insulin effect on lipolysis is what is critical for determination of glucose output in the fasting state, and that insulin resistance at the level of the adipocyte may determine the extent of fasting hyperglycaemia, and may be an important factor in the overall phenotype in prediabetic and NIDDM individuals.

Animals↗