Background Improved blood-glucose control decreases the progression of diabetic microvascular disease, but the effect on macrovascular complications is unknown. There is concern that sulphonylureas may increase cardiovascular mortality in patients with type 2 diabetes and that high insulin concentrations may enhance atheroma formation. We compared the effects of intensive blood-glucose control with either sulphonylurea or insulin and conventional treatment on the risk of microvascular and macrovascular complications in patients with type 2 diabetes in a randomised controlled trial.Methods 3867 newly diagnosed patients with type 2 diabetes, median age 54 years (IQR 48-60 years), who after 3 months' diet treatment had a mean of two fasting plasma glucose (FPG) concentrations of 6.1-15.0 mmol/L were randomly assigned intensive policy with a sulphonylurea (chlorpropamide, glibenclamide, or. glipizide) or with insulin, or conventional policy with diet. The aim in the intensive group was FPG less than 6 mmol/L. in the conventional group, the aim was the best achievable FPG with diet atone; drugs were added only if there were hyperglycaemic symptoms or FPG greater than 15 mmol/L. Three aggregate endpoints were used to assess differences between conventional and intensive treatment: any diabetes-related endpoint (sudden death, death from hyperglycaemia or hypoglycaemia, fatal or non-fatal myocardial infarction, angina, heart failure, stroke, renal failure, amputation [of at least one digit], vitreous haemorrhage, retinopathy requiring photocoagulation, blindness in one eye,or cataract extraction); diabetes-related death (death from myocardial infarction, stroke, peripheral vascular disease, renal disease, hyperglycaemia or hypoglycaemia, and sudden death); all-cause mortality. Single clinical endpoints and surrogate subclinical endpoints were also assessed. All analyses were by intention to treat and frequency of hypoglycaemia was also analysed by actual therapy.Findings Over 10 years, haemoglobin A(1c) (HbA(1c)) was 7.0% (6.2-8.2) in the intensive group compared with 7.9% (6.9-8.8) in the conventional group-an 11% reduction. There was no difference in HbA(1c) among agents in the intensive group. Compared with the conventional group, the risk in the intensive group was 12% lower (95% CI 1-21, p=0.029) for any diabetes-related endpoint; 10% lower (-11 to 27, p=0.34) for any diabetes-related death; and 6% lower (-10 to 20, p=0.44) for all-cause mortality. Most of the risk reduction in the any diabetes-related aggregate endpoint was due to a 25% risk reduction (7-40, p=0.0099) in microvascular endpoints, including the need for retinal photocoagulation. There was no difference for any of the three aggregate endpoints the three intensive agents (chlorpropamide, glibenclamide, or insulin).Patients in the intensive group had more hypoglycaemic episodes than those in the conventional group on both types of analysis (both p<0.0001). The rates of major hypoglycaemic episodes per year were 0.7% with conventional treatment, 1.0% with chlorpropamide, 1.4% with glibenclamide, and 1.8% with insulin. Weight gain was significantly higher in the intensive group (mean 2.9 kg) than in the conventional group (p<0.001), and patients assigned insulin had a greater gain in weight (4.0 kg) than those assigned chlorpropamide (2.6 kg) or glibenclamide (1.7 kg).Interpretation Intensive blood-glucose control by either sulphonylureas or insulin substantially decreases the risk of microvascular complications, but not macrovascular disease, in patients with type 2 diabetes. None of the individual drugs had an adverse effect on cardiovascular outcomes. All intensive treatment increased the risk of hypoglycaemia.

The excess of coronary heart disease in Indian Asians compared with Europeans is unexplained by conventional risk factors, although the high prevalence of diabetes may play a part.To explore the contribution of diet we compared the fatty acid composition of erythrocyte membrane phospholipid and plasma triglyceride in 36 Gujarati Asians and 24 Europeans with non-insulin-dependent diabetes. Erythrocytes from Asian subjects contained higher proportions of linoleic, dihomogammalinolenic, and arachidonic acids, and lower proportions of oleic and n-3 series fatty acids; triglycerides contained higher linoleic and lower oleic acid levels. For example, mean percentage (SE) of oleic acid (18:1n-9) in erythrocytes was 16.7 (0.2) in Asians and 20.5 (0.6) in Europeans (p=0.0001), and total n-6:n-3 ratio was, respectively, 12.8 (0.7) and 6.7 (0.7) (p=0.0001).A high dietary intake of linoleic acid may not be cardioprotective unless balanced by significant intakes of oleic and n-3 series fatty acids, at least in diabetic Indian Asians, By itself, the conventional recommendation to substitute polyunsaturated for saturated fat in the diet may be inadequate to reduce thrombogenesis, and the overall balance of fatty acids, including monounsaturates, should be considered.

ABSTRACTA batch of frozen concentrated grapefruit juice (GJ) was reconstituted to 10° Brix with water and adjusted with sucrose, citric acid and/or deacidified GJ to produce five experimental samples with Brix:acid ratios from 7–15. Consumers from four large U.S. cities evaluated the samples for flavor, preference and five other quality attributes. Flavor means varied within an acceptable range. Preference was for samples in the 8.4 to 11.1 ratio range. Nonusers preferred 11.1 ratio juice and rated the three lowest ratio juices lower than users. As ratio increased, consumer perception of sweetness increased and decreased for tartness, bitterness, and aroma. All samples were judged somewhat too tart and bitter (except at 15 ratio) and not quite sweet enough.

ABSTRACTFlavor evaluations are presented for two samples of frozen concentrated orange juice (FCOJ). Each sample of 42°Brix commercial type FCOJ was prepared by blending concentrates of juices of four cultivars (27% Hamlin, 20% Pineapple, 50% Valencia and 3% Murcott). One sample was made only with concentrates from low yield juices of each cultivar and the other sample was made only from concentrates from high yield juices of the four cultivars. Both the samples were rated very good flavor when graded according to USDA standards for grades of FCOJ, but showed lower scores for high yield than for low yield juices. Results of six industry flavor panel evaluations are presented.

ABSTRACTControlling viscosity is critical to efficient evaporation and pumping of citrus concentrates. Viscosity was reduced by a commercial homogenizer installed between the third and fourth stage of a pilot plant TASTE evaporator. Juice was concentrated to 65°Brix with and without homogenization. The results showed a 13% decrease in viscosity due to homogenization. Mean non‐homogenized values were 279 mPa.s (s.d. = 7.5) on the 65°Brix control and 242 mPa.s (s.d. = 10) on the homogenized concentrate, both measured at 3.50 set1, which was calculated to be the shear rate for these samples within the third stage of this evaporator. This decrease in viscosity also reduced the energy consumption about 3 to 4% or produced a higher (2 to 3) °Brix concentrate. Homogenization did not significantly affect the juice color, acid, pulp or vitamin C.

ADP-induced platelet aggregation was measured in 15 Type 1 (insulin-dependent) diabetic patients, 15 Type 2 (non-insulin-dependent) diabetic patients and in 15 non-diabetic control subjects. Simultaneous measurements were made of fasting blood glucose, glycosylated haemoglobin, serum insulin, total plasma cholesterol, cholesterol in the lipoprotein subfractions, total triglycerides and platelet phospholipid fatty acid levels. Regression analysis of aggregation against the biochemical variables within the three groups revealed that there was no significant difference in the associations with aggregation between the groups. When the data was pooled, blood glucose (p<0.01) and glycosylated haemoglobin (p<0.05) demonstrated significant associations with aggregation. Multiple regression analysis was then applied; only blood glucose (p<0.05) had an independent effect on aggregation. Platelet aggregation in diabetic patients and non-diabetic patients appears to be related directly only to blood glucose levels.

We measured the platelet total phospholipid fatty acid profiles of 20 insulin treated (Type I) diabetics, 20 non-insulin treated (Type II) diabetics and 20 matched non-diabetic controls to determine the relationship between the omega 6 and omega 3 series of fatty acids in diabetes. A significant inverse correlation between linoleic acid and arachidonic acid occurred in the normal subjects (r = -0.61; P less than 0.001) but was not seen in the Type I diabetics (r = -0.13; P = NS) or in the Type II diabetics (r = -0.27; P = NS). No significant correlation was seen between linolenic acid and eicosapentaenoic acid in the normal controls (r = -0.34; P = NS) or in the Type I diabetics (r = 0.21; P = NS) or in the Type II diabetics (r = -0.20; P = NS). The results suggest that a functional impairment of platelet delta 5 and delta 6 desaturase may occur in diabetes which disrupts the normal equilibrium between linoleic acid and arachidonic acid. However, the level of eicosapentaenoic acid appears to be less dependent on conversion from linolenic acid. Our findings are of importance to studies designed to reduce platelet aggregation in diabetics and non-diabetics by manipulation of the levels of the precursor fatty acids of thromboxane.

The effects of regularly eating sucrose were studied in 23 diabetic patients, 12 Type 1 (insulin-dependent) and 11 Type 2 (non-insulin-dependent), with differing degrees of glycaemic control. Two diets, each lasting 6 weeks, were compared in a randomised cross-over study. Both diets were high in fibre and low in fat. In one diet 45 g of complex carbohydrate was replaced by 45 g of sucrose taken at mealtimes. There were no significant biochemical differences between the two diets in either Type 1 or Type 2 patients. In Type 1 patients the mean (±SEM) fasting plasma glucose was 10.5 (1.8) mmol/1 on the control diet and 10.3 (1.5) mmol/1 on sucrose. In Type 2 patients the levels were 9.1 (0.8) mmol/1 and 8.9 (0.8) mmol/l respectively. Glycosylated haemoglobin for the Type 1 patients was 9.9% on control and 10.3% on sucrose; for Type 2 patients the figures were 9.3% and 9.0% respectively. There were no differences in mean daily plasma glucose levels or diurnal glucose profiles. Cholesterol (total and in lipoprotein fractions) was unchanged, as were diurnal triglyceride profiles and plasma insulin profiles in the Type 2 patients. There were no changes in medication or body weight. We conclude that a moderate amount of sucrose taken daily at mealtimes does not cause deterioration in metabolic control in diabetic patients following a high fibre/low fat diet.

A group of non-insulin dependent diabetics taking oral hypoglycaemic therapy were studied to determine the effect of improved diabetic control on the platelet levels of the prostaglandin precursor fatty acids. The patients were randomised to receive either a low carbohydrate diet (35% of total energy) for six weeks or a high carbohydrate diet (55% of total energy), high fibre diet for six weeks and the diets were then reversed. At the end of the high carbohydrate, high fibre diet the mean fasting blood glucose (6.6 mmol section 1) and mean percentage glycosylated haemoglobin (8.2%) were significantly lower than after the low carbohydrate diet (7.8. mmol/l, p less than 0.05: 9.9%, p less than 0.01). Mean platelet phospholipid arachidonic acid percentage was significantly higher after the high carbohydrate, high fibre diet (24.2%) than after the low carbohydrate diet (19.9%, p less than 0.01). There were no significant changes in the other platelet fatty acids.

Platelet aggregation was measured in 15 patients having non‐insulin‐dependent diabetes mellitus (NIDDM) at the time of diagnosis and after three months of dietary treatment. Mean fasting plasma glucose fell from 13.0 to 8.8 mmol/l (p<0.0002), glycosylated haemoglobin fell from a mean of 11.3% to 9.0% (p<0.005) and insulin levels fell from a mean of 17.5 to 13.8 mU/l (p<0.005). Platelet aggregation showed a variable response and did not correlate with plasma glucose, glycosylated haemoglobin or plasma insulin. Multiple linear regression analysis was carried out on the aggregation values against the biochemical variables and platelet phospholipid fatty acid levels following logarithm transformation. Platelet linolenic acid and eicosapentaenoic acid levels were significantly inversely associated with aggregation but the difference between the relationship at diagnosis and after three months was not statistically significant. The association between platelet w3 fatty acids and platelet aggregation suggest that dietary change aimed at increasing the proportions of these fatty acids might favourably influence vascular disease in NIDDM via an effect on platelet function.

Twenty diabetic outpatients (12 non-insulin-treated and 8 insulin-treated) were given guar granulate in a dose of 10 g daily for two months in order to study the effect on glycaemic control and lipid levels. Mean glycosylated haemoglobin levels (HbA1c%) fell from 11.1 +/- 2.0% pre-guar to 10.5 +/- 2.2% (P less than 0.001) after one month on guar and to 10.1 +/- 2.3% (P less than 0.0001) after two months. Following discontinuation of guar, HbA1c% rose to 11.1 +/- 2.5% (P less than 0.002). However, there were no significant changes in fasting blood glucose, 1 h postprandial blood glucose following a test meal, 24 h urinary glucose excretion or in lipid levels. Gastrointestinal side effects occurred in 4 patients during treatment with guar. Four patients reduced their dose of insulin and 2 patients reduced their dose of sulphonylurea therapy during this time because of symptoms suggestive of hypoglycaemia. We suggest that the low dose of guar used in this study may help improve glycaemic control in diabetic patients and that this may be achieved with a low incidence of gastrointestinal side effects.

One hundred and forty nine diabetic patients were ophthalmologically assessed seven years after randomisation to a low carbohydrate or modified fat diet (rich in linoleic acid). Glycaemic control, regardless of the type of diet, was a major determinant of the development of retinopathy. Poorly controlled patients (haemoglobin A1c greater than 8%) with low levels of linoleic acid in cholesterol ester had a significantly greater frequency of retinopathy than well controlled patients or patients with similarly unsatisfactory control but higher levels of linoleic acid. The findings support an earlier suggestion that linoleic acid might protect against diabetic retinopathy.

Platelet aggregation, platelet prostaglandin precursor fatty acids, glycaemia and lipid levels were studied in a group of insulin dependent diabetics whilst taking Aspirin (900 mg daily) and Dipyridamole (300 mg daily) and again two months after discontinuing this treatment.

The effects of slip character and grain size on the intrinsic material and extrinsic closure contributions to fatigue crack growth resistance have been studied for a 7475 aluminum alloy. The alloy was tested in the underaged and overaged conditions with grain sizes of 18 μm and 80 μm. The fracture surface exhibited increased irregularity and planar facet formation with increased grain size, underaging, and tests in vacuum. These changes were accompanied by an increased resistance to fatigue crack growth. In air the 18 μm grain size overaged material exhibited relatively poor resistance to fatigue crack growth compared with other microstructural variants, and this was associated with a lower stress intensity for closure. All materials exhibited a marked improvement in fatigue crack growth resistance when tested in vacuum, with the most significant difference being ˜1000× at a ΔK of 10 MPa m1/2 for the 80 μm grain size underaged alloy. This improvement could not be accounted for by either an increase in closure or increased crack deflection and is most likely due to increased slip reversibility in the vacuum environment. The intrinsic resistance of the alloy to fatigue crack growth was microstructurally dependent in vacuum, with large grains and planar slip providing the better fatigue performance.

Twelve patients with familial hypercholesterolaemia (FH) who had not achieved satisfactory cholesterol levels on dietary advice alone were treated with cholestyramine for 6 months and probucol for 6 months in a randomised cross-over study to compare the relative effectiveness of the two drugs.

Fifteen non‐insulin‐dependent diabetic patients with persistently elevated blood glucoses despite high doses of oral hypoglycaemic agents, were randomly allocated to a high carbohydrate‐high fibre diet (HC) or a reinforced low carbohydrate diet (LC). After six weeks the diets were reversed for a similar period. Immediately preceding the study and at the end of each dietary period 24‐h biochemical profiles were performed. In the 11 patients who completed the study, fasting and preprandial glucose, percentage glycosylated haemoglobin, VLDL cholesterol and mean 24‐h triglycerides were significantly lower on HC than on LC or during the initial profile on their usual diet. There was no significant difference in any of the measurements on LC compared with the usual diet. Previous studies of high carbohydrate‐high fibre diets in diabetes have been carried out in relatively well‐controlled patients. These data show that poorly controlled non‐insulin‐dependent patients have an even more striking response.

Ten diabetic patients were given test meals at breakfast and lunch on successive days to compare the acute glycaemic responses to meals either high (65%) (HC) or extremely low (12%) in carbohydrate; the latter was very high (71%) in fat (HF). The meals were isocaloric and fibre content, though higher in HC, was within the range of the average British intake for both diets. The mean fasting blood glucose levels were similar on the 2 days (9.8 mmol/l; 9.6 mmol/l) but mean peak post-prandial levels were significantly greater after the HC meals (17.7 mmol/l after breakfast and 14.1 mmol/l after lunch) than after the HF meals (11.7 mmol/litre after breakfast; P less than 0.02; 8.1 mmol/l after lunch; P less than 0.02). Mean blood glucose value for the 6-hr study period was significantly higher after the HC meals (14.0 mmol/l) than after the HF meals (9.2 mmol/l; P less than 0.001). There was no significant difference in mean fasting, peak or total mean triglyceride level. In the short term, therefore, meals very low in carbohydrate and high in fat are followed by a lower glycaemic response than meals high in carbohydrate but with only a usual (22 g/day) fibre content. Delayed gastric emptying after HF meals may well contribute to the results but long-term use of such HF meals is not advised in view of the extremely high fat content.

1. Two groups of patients with non-insulin-dependent diabetes mellitus (NIDDM), with dietary advice randomized between a low-carbohydrate (LC) diet and a modified-fat (MF) diet, were followed to determine the effect of diet on phospholipid fatty acid composition of platelets and on development of retinopathy in the 7 years following diagnosis. There was a tendency for retinopathy to occur more frequently in those randomiEd to the LC diet. This difference was not statistically significant, and fatty acid composition of platelets did not differ significantly in those with and without retinopathy.2. Linoleic acid values from platelet phospholipid fatty acids were significantly higher in NIDDM on an MF diet compared with an LC diet.3. There was no difference between the two dietary subgroups with respect to platelet arachidonic acid, but this was lower in the whole diabetic population when compared with non-diabetics.4. The arachidonic acid values correlated with neither glycosylated haemoglobin nor mean glycaemia.5. Significant correlation between the fatty acid values for platelets and plasma cholesterol esters was found only for 16:0.

Conference Abstract| December 01 1984 Platelet Aggregation in Type 2 (Non-Insulin Dependent) Diabetes is Associated with Plasma Cholesterol and Platelet Fatty Acids D.B. Jones; D.B. Jones 1Diabetes Research Laboratories and Department of Community Medicine and General Practice, Radcliffe Infirmary, Oxford Search for other works by this author on: This Site PubMed Google Scholar B. Haitas; B. Haitas 1Diabetes Research Laboratories and Department of Community Medicine and General Practice, Radcliffe Infirmary, Oxford Search for other works by this author on: This Site PubMed Google Scholar E.G. Bown; E.G. Bown 1Diabetes Research Laboratories and Department of Community Medicine and General Practice, Radcliffe Infirmary, Oxford Search for other works by this author on: This Site PubMed Google Scholar R.D. Carter; R.D. Carter 1Diabetes Research Laboratories and Department of Community Medicine and General Practice, Radcliffe Infirmary, Oxford Search for other works by this author on: This Site PubMed Google Scholar K. Barker; K. Barker 1Diabetes Research Laboratories and Department of Community Medicine and General Practice, Radcliffe Infirmary, Oxford Search for other works by this author on: This Site PubMed Google Scholar R. Jelfs; R. Jelfs 1Diabetes Research Laboratories and Department of Community Medicine and General Practice, Radcliffe Infirmary, Oxford Search for other works by this author on: This Site PubMed Google Scholar R.C. Turner; R.C. Turner 1Diabetes Research Laboratories and Department of Community Medicine and General Practice, Radcliffe Infirmary, Oxford Search for other works by this author on: This Site PubMed Google Scholar J.I. Mann J.I. Mann 1Diabetes Research Laboratories and Department of Community Medicine and General Practice, Radcliffe Infirmary, Oxford Search for other works by this author on: This Site PubMed Google Scholar Clin Sci (Lond) (1984) 67 (s9): 66P–67P. https://doi.org/10.1042/cs067066Pb Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation D.B. Jones, B. Haitas, E.G. Bown, R.D. Carter, K. Barker, R. Jelfs, R.C. Turner, J.I. Mann; Platelet Aggregation in Type 2 (Non-Insulin Dependent) Diabetes is Associated with Plasma Cholesterol and Platelet Fatty Acids. Clin Sci (Lond) 1 December 1984; 67 (s9): 66P–67P. doi: https://doi.org/10.1042/cs067066Pb Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search This content is only available as a PDF. © 1984 The Biochemical Society and the Medical Research Society1984 Article PDF first page preview Close Modal You do not currently have access to this content.