scispace - formally typeset
Search or ask a question

Showing papers by "K. G. M. M. Alberti published in 1998"


Journal ArticleDOI
TL;DR: A WHO Consultation has taken place in parallel with a report by an American Diabetes Association Expert Committee to re‐examine diagnostic criteria and classification of diabetes mellitus and is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.
Abstract: The classification of diabetes mellitus and the tests used for its diagnosis were brought into order by the National Diabetes Data Group of the USA and the second World Health Organization Expert Committee on Diabetes Mellitus in 1979 and 1980. Apart from minor modifications by WHO in 1985, little has been changed since that time. There is however considerable new knowledge regarding the aetiology of different forms of diabetes as well as more information on the predictive value of different blood glucose values for the complications of diabetes. A WHO Consultation has therefore taken place in parallel with a report by an American Diabetes Association Expert Committee to re-examine diagnostic criteria and classification. The present document includes the conclusions of the former and is intended for wide distribution and discussion before final proposals are submitted to WHO for approval. The main changes proposed are as follows. The diagnostic fasting plasma (blood) glucose value has been lowered to > or =7.0 mmol l(-1) (6.1 mmol l(-1)). Impaired Glucose Tolerance (IGT) is changed to allow for the new fasting level. A new category of Impaired Fasting Glycaemia (IFG) is proposed to encompass values which are above normal but below the diagnostic cut-off for diabetes (plasma > or =6.1 to or =5.6 to <6.1 mmol l(-1)). Gestational Diabetes Mellitus (GDM) now includes gestational impaired glucose tolerance as well as the previous GDM. The classification defines both process and stage of the disease. The processes include Type 1, autoimmune and non-autoimmune, with beta-cell destruction; Type 2 with varying degrees of insulin resistance and insulin hyposecretion; Gestational Diabetes Mellitus; and Other Types where the cause is known (e.g. MODY, endocrinopathies). It is anticipated that this group will expand as causes of Type 2 become known. Stages range from normoglycaemia to insulin required for survival. It is hoped that the new classification will allow better classification of individuals and lead to fewer therapeutic misjudgements.

15,167 citations


Journal ArticleDOI
TL;DR: Despite the lack of change in fasting plasma NEFA levels, acipimox caused a modest beneficial improvement in overall glycemic control and plasma lipids in NIDDM patients and could be a useful agent in the treatment of dyslipidemic NID DM patients.
Abstract: Elevated circulating plasma nonesterified fatty acids (NEFA) may contribute to the insulin resistance and hyperglycemia of non—insulin-dependent diabetes mellitus (NIDDM), and decreasing plasma NEFA could provide a therapeutic benefit. A sustained-release preparation of acipimox, a lipolysis inhibitor, was used in an attempt to decrease circulating plasma NEFA levels long-term, and the effects on glycemic control, insulin resistance, and serum lipids were measured. Sixty NIDDM patients (43 males and 17 females) took part in a randomized controlled trial of acipimox or placebo for 12 weeks. Fasting plasma NEFA levels did not change in acipimox-treated patients (baseline v 12 weeks, 0.84 ± 0.35 v 0.88 ± 0.55 mmol · L−1, mean ± SD). Fasting blood glucose was unchanged (mean difference v placebo, −0.5 mmol · L−1; 95% confidence interval [CI], −1.4 to 0.3 mmol · L−1), but serum fructosamine decreased (mean difference v placebo, −26 μmol · L−1; 95% CI, −51 to 0 mmol · L−1), as did the standardized hemoglobin A1 ([HbA1] mean difference v placebo, −1.4%; 95% CI, −3.0% to −0.1%). Insulin resistance measured as steady-state plasma glucose during an insulin-dextrose infusion test was unchanged (mean difference v placebo, −1.4 mmol · L−1; 95% CI, −3.2 to 0.5 mmol · L−1). Serum total cholesterol (mean difference v placebo, −0.4 mmol · L−1; 95% CI, −0.6 to −0.1 mmol · L−1), serum apolipoprotein B ([apo B] mean difference v placebo, −0.19 g · L−1; 95% CI, −0.3 to −0.1 g · L−1), and serum triglycerides (mean difference v placebo for pretreatment v posttreatment ratio, 0.59; 95% CI, 0.40 to 0.88) were all lower with acipimox. Serum high-density lipoprotein (HDL) cholesterol (mean difference v placebo, 0.10 mmol · L−1; 95% CI, −0.05 to 0.3 mmol · L−1), serum apo A1 (mean difference v placebo, 0.03 g · L−1; 95% CI, −0.04 to 0.1 g · L−1), and serum lipoprotein(a) ([Lp(a)] acipimox v placebo, 154 (0 to 1,574) v 71 (0 to 1,009), median and range) were unchanged. Despite the lack of change in fasting plasma NEFA levels, acipimox caused a modest beneficial improvement in overall glycemic control and plasma lipids in NIDDM patients and could be a useful agent in the treatment of dyslipidemic NIDDM patients.

16 citations


Journal ArticleDOI
TL;DR: Glucokinase is dramatically suppressed in liver disease, which although partly compensated for by the increase in hexokinase I (and II), accounts in part for the well-known glucose intolerance of liver cirrhosis.

16 citations