Effect of intensive dietetic interventions on weight and glycaemic control in overweight men with Type II diabetes: a randomised trial

2003 ◽  
Vol 27 (7) ◽  
pp. 797-802 ◽  
Author(s):  
S Ash ◽  
M M Reeves ◽  
S Yeo ◽  
G Morrison ◽  
D Carey ◽  
...  
1996 ◽  
Vol 89 (1) ◽  
pp. 27-30 ◽  
Author(s):  
B J Boucher ◽  
J Tsoumanis ◽  
K Noonan ◽  
J Holmes

Glycosylated haemoglobins and weights were recorded for 200 consecutive diabetic clinic attendere seen yearly for 5 years, 76 of whom were also seen up to 10 years from diagnosis of type 2 diabetes, representing 1380 patient years. Weight fluctuation (≥3 kg) was associated with increased final prevalence of hypertension, macroalbuminaemia and a raised creatinine (P≤ 0.002) but this relationship was abolished by correction for higher initial weight. Average giycaemia over 5/10 years [itself related to initial weight in women on tablets (N=53) but not others, and to waist but not waist/hip ratio], correlated with prevalence and severity of retinopathy (N=200; r=0.38, P≤0.0006) seen also in the subgroup of patients on tablets (N=145, P≤0.006). At HbA1 levels ≥10.5% an increased prevelance of retinopathy was seen in those on insulin (W=37, P≤0.001) and an increased prevalence of peripheral vascular disease was seen in men but not women (x2=2.87, P≤0.01) as well as in the prevalence of neuropathy. These findings suggest that good glycaemic control is of value in type 2 diabetes and less easily achieved in obesity.


2000 ◽  
Vol 98 (3) ◽  
pp. 355-363 ◽  
Author(s):  
Bharti MACKNESS ◽  
Paul N. DURRINGTON ◽  
Bashir ABUASHIA ◽  
Andrew J. M. BOULTON ◽  
Michael I. MACKNESS

Human serum paraoxonase 1 (PON1) is located on high-density lipoprotein and has been implicated in the detoxification of organophosphates, and possibly in the prevention of lipid peroxidation of low-density lipoprotein. PON1 has two genetic polymorphisms, both due to amino acid substitutions: one involving glutamine (Q genotype) and arginine (R genotype) at position 192, and the other involving leucine (L genotype) and methionine (M genotype) at position 55. We investigated the effects of these polymorphisms, and of a polymorphism of the PON2 gene at position 310 (Cys/Ser; C and S genotypes respectively), on serum PON1 activity and concentration, plasma lipids and lipoproteins and glycaemic control in 93 individuals with type II diabetes with no complications and in 101 individuals with type II diabetes with retinopathy. Serum PON1 activity in the group with no complications [median 164.1 nmol·min-1·ml-1 (range 8.0–467.8)] was significantly higher than in the group with retinopathy [113.4 nmol·min-1·ml-1 (3.0–414.6)] (P< 0.001), but the serum PON1 concentration was not different between the groups. The gene frequencies of the PON1-55 and PON1-192 polymorphisms and of the PON2-310 polymorphism were not different between the study populations. The PON1-55 and PON1-192 polymorphisms affected PON1 activity in the way described in a previous study of a control group and subjects with type II diabetes. The PON2-310 polymorphism also significantly affected serum PON1. PON1 activity was significantly higher in individuals with the PON2-310 CC genotype in both groups with type II diabetes, and the PON1 concentration was significantly higher in PON2-310 CC homozygotes with no complications than in the group with retinopathy. Neither the PON1-55 nor the PON1-192 polymorphism was correlated with the serum lipid or lipoprotein concentration in either group. In the group with retinopathy (but not the group with no complications), all three PON polymorphisms were correlated with glycaemic control, which was worse for the PON1-55 genotypes in the order MM > LM > LL (P = 0.0032), for the PON1-192 genotypes in the order RR > QR > QQ (P = 0.011) and for the PON2-310 genotypes in the order CC > CS > SS (P = 0.010). Low serum PON1 activity in retinopathy may be related to an increased tendency for lipid peroxidation. Our findings thus raise the possibility that, in retinopathy, the PON2 gene may influence PON1, and that an inter-relationship between the PON1 and PON2 genes may influence glycaemic control in subjects with type II diabetes complicated by retinopathy.


2006 ◽  
Vol 111 (2) ◽  
pp. 119-126 ◽  
Author(s):  
Stephan F. E. Praet ◽  
Ralph J. F. Manders ◽  
Ruth C. R. Meex ◽  
A. G. Lieverse ◽  
Coen D. A. Stehouwer ◽  
...  

The aim of the present study was to assess the level of glycaemic control by the measurement of 24 h blood glucose profiles and standard blood analyses under identical nutritional and physical activity conditions in patients with Type II diabetes and healthy normoglycaemic controls. A total of 11 male patients with Type II diabetes and 11 healthy matched controls participated in a 24 h CGMS (continuous subcutaneous glucose-monitoring system) assessment trial under strictly standardized dietary and physical activity conditions. In addition, fasting plasma glucose, insulin and HbA1c (glycated haemoglobin) concentrations were measured, and an OGTT (oral glucose tolerance test) was performed to calculate indices of whole-body insulin sensitivity, oral glucose tolerance and/or glycaemic control. In the healthy control group, hyperglycaemia (blood glucose concentration >10 mmol/l) was hardly present (2±1% or 0.4±0.2/24 h). However, in the patients with Type II diabetes, hyperglycaemia was experienced for as much as 55±7% of the time (13±2 h over 24 h) while using the same standardized diet. Breakfast-related hyperglycaemia contributed most (46±7%; P<0.01 as determined by ANOVA) to the total amount of hyperglycaemia and postprandial glycaemic instability. In the diabetes patients, blood HbA1c content correlated well with the duration of hyperglycaemia and the postprandial glucose responses (P<0.05). In conclusion, CGMS determinations show that standard measurements of glycaemic control underestimate the amount of hyperglycaemia prevalent during real-life conditions in Type II diabetes. Given the macro- and micro-vascular damage caused by postprandial hyperglycaemia, CGMS provides an excellent tool to evaluate alternative therapeutic strategies to reduce hyperglycaemic blood glucose excursions.


Diabetologia ◽  
2000 ◽  
Vol 43 (4) ◽  
pp. 411-415 ◽  
Author(s):  
N. Ueno ◽  
A. Inui ◽  
A. Asakawa ◽  
F. Takao ◽  
S. Tani ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document