Recently, high carbohydrate diets were recommended for the treatment of diabetes mellitus. All aspects of these diets, however, have not been fully tested — particularly in insulin dependent diabetes mellitus (IDDM). The present study was designed to investigate the effects of high carbohydrate, low fat diets (HCLFD) on blood glucose regulation, lipoprotein and apoprotein concentrations and nutritional status in IDDM. Six women with IDDM were studied in the Clinical Research Center for ten weeks. The study was divided into a control diet (CD) with 45% CHO, 40% fat, and 15% protein for four weeks, and a HCLFD with 65% CHO, 20% fat, and 15% protein for six weeks. Subjects were allowed free selection of their carbohydrate and fiber sources during both diet periods. The resulting selections produced diets with approximately equal proportions of complex and simple carbohydrates (49% and 51%, respectively) and moderate quantities of dietary fiber (50 g) during the HCLFD. Weekly fasting and pre-prandial serum glucose and glycosylated hemoglobin, and daily 24 hr. urine glucose excretion and insulin dose were not significantly different between the two periods. Total plasma, LDL and HDL cholesterol concentrations (p<.05). and apopproteins AI (p<.001), B (p<.01) and CIII (p<.05) were significantly lower, VLDL cholesterol (p<.05), total plasma (p<.01) and VLDL (p<.001) triglycerides were significantly higher, and apoproteins AII and E were unchanged during the HCLFD. Lipoprotein and apoprotein concentrations were independent of glycemic control. There were no significant changes in any of the nutritional parameters tested. All except vitamin B₆ were within their respective normal ranges. Whole blood and plasma vitamin B₆, and pyridoxal 5'-phosphate fell below the lower limits, even though dietary intakes were adequate. The present study suggest that HCLFD did not adversely affect glycemic control in IDDM, and demonstrated a potentially beneficial lowering of total and LDL cholesterol concentrations independent of glycemic control. Finally, nutritional status appeared unaltered as a result of HCLFD. The lower levels of the B₆ vitamers in IDDM demonstrated in this study suggest that the relationship between diabetes and vitamin B₆ status needs to be investigated further. / Graduation date: 1982

Call number: LD2668 .T4 1954 B5 / Master of Science

No description available.

The independent effect of a high polyunsaturated:saturated fat (P:S) diet on glycemic control in humans has been poorly studied. We propose that a P:S $>$ 1.0 vs P:S 1.0 vs. P:S 1.0. HDL and IGFl were significantly lower with the P:S $>$ 1.0. Si was unaffected by the P:S difference, however, trends towards decreased Sg and increased insulin secretion were seen with P:S $>$ 1.0. The small sample size limits the making of firm conclusions, however, it suggests that glycemic control may be improved through increased insulin secretion a result of an increase in P:S.

The status of vitamin B-6 (B6) nutriture of nine persons (4F;5M) with insulin dependent diabetes mellitus (IDDM), nine persons (5F;4M) with non-insulin dependent diabetes mellitus (NIDDM), and 18 control individuals (9F;9M) was evaluated, using biochemical and dietary indicators of B6 status. The biochemical indices employed were plasma concentration of pyridoxal 5'-phosphate (PLP), urinary 4-pyridoxic acid (4PA) excretion, and urinary kynurenic acid (KA) and xanthurenic, acid (XA) excretion following a tryptophan load test (2 g L-tryptophan oral load). Dietary B6 intake and the ratio of B6 (mg) to dietary protein (g) (B6:protein) were determined. Fasting blood, two consecutive 24 h urine collections and three consecutive daily weighed diet records were obtained on each of two occasions, separated by 30-70 d. Diet records were analyzed for vitamin B-6 and protein intake using nutrient data bases. Samples of 70 foods, for which the data bases lacked B6 values, were obtained and analyzed for total B6 content by a microbiological method. The plasma concentration of PLP was determined by an enzymatic method, and plasma alkaline phosphatase activity by a colorimetric method. Urinary 4PA was separated by HPLC, urinary KA and XA by ion exchange, and each metabolite was determined fluorometrically. The mean daily vitamin B-6 intake of each group exceeded the recommended dietary allowance (RDA). The mean B6:protein ratios ± standard deviations (SD) for the groups of females were 0.0200±0.0027, 0.0304±0.0101, and 0.0254±0.0099 for IDDM, NIDDM and control (C), respectively. The respective B6:protein ratios for the males were 0.0280±0.0040, 0.0242±0.0038 and 0.0241±0.0078. The mean±SD plasma PLP concentrations for females were 22.4±6.8, 21.8±9.6 and 37.4126.8 nmol/L for IDDM, NIDDM and C, respectively. The mean plasma PLP concentrations of the two groups of females with diabetes were at the low end of a range (22.4-25.3 nmol/L) suggested to indicate marginal status, and 56% of the females with diabetes had PLP concentrations below the lower boundary of the marginal range. For the three groups of males the PLP concentrations were in the same rank order as dietary B6 intake; 53.9±18.2, 43.6±7.2 and 37.5±17.7 nmol/L for IDDM, NIDDM and C, respectively. Plasma PLP concentration was strongly and significantly correlated with B6 intake in both diabetes (n=18, r=.744, p<.001) and C (n=18, r=.695, p<.001) groups, but was also negatively associated with plasma AP activity only for the diabetes group (n=18, r=- .454, a=.058). The mean plasma AP activity of females with NIDDM was significantly higher than that of the female C group (p<.01). Greater than normal AP hydrolysis of PLP is thought to have contributed to the low plasma PLP concentrations observed in the females with NIDDM. Levels of urinary 4PA excretion by females were 8.76±2.10, 7.61±12.57 and 8.15±14.43 μmol/d for IDDM, NIDDM and C, respectively, or 87, 63 and 72% of B6 intake. For males the urinary 4PA levels were 12.76±14.53, 10.32±11.77 and 9.81+3.34 μmol/d, respectively, or 76, 68 and 78% of B6 intake. All subjects excreted 4-PA in amounts indicative of adequate B6 status. All means for tryptophan metabolites were within ranges seen for normal subjects, both pre and post-tryptophan load. None of the subjects with diabetes and only one female C subject excreted more than 65 μmol XA in 24 h after the tryptophan load (upper boundary of normal response to 2 g tryptophan load). Mean post-load excretion of XA and KA of diabetes groups was numerically lower than that of same sex controls in all comparisons, although in only one instance was the difference significant (NIDDM females post-load KA, p<.05). The results of the tryptophan load test suggest adequate B6 function in the kynurenine pathway those with diabetes and controls. Individuals with diabetes were found to consume adequate or above amounts of B6 by the standard of the RDA. Low plasma PLP levels were observed in females with IDDM who had the lowest B6 intake, and in females with NIDDM who had the highest plasma AP activity. The present research indicates that low PLP may be present in diabetes, as observed by other investigators, despite seemingly adequate B6 nutriture. However, normal to above normal amounts of urinary 4-PA excretion indicated adequate body stores of B6, and normal response to the tryptophan load test suggested adequate function of B6 in the liver of persons with diabetes. Plasma PLP concentration alone may not be an adequate B6 status indicator in persons with diabetes. Based upon the levels of multiple indicators, the vitamin B-6 status of those persons with diabetes studied was judged to be adequate. / Graduation date: 1991

No description available.

No description available.

The objective of this study was to determine if teaching the new sugar guidelines, which now permit up to 10% of energy from added sugars, would modify dietary habits, metabolic control and perceived quality of life in free-living subjects with type 2 diabetes. In an eight month randomized controlled trial, 48 subjects with type 2 diabetes were taught, by a trained dietitian, either a conventional diabetic meal plan: conventional group (C) or one in which they could integrate the new sugar guidelines: sugar group (S). Patients were seen at the clinic every 2 months (total of 5 visits) by the dietitian and the endocrinologist. During the pre-randomization period (0 to 4 months) all subjects were taught the conventional diabetic diet and advised to avoid concentrated sugars. Randomization to the C or the S group took place at the 4 month visit (4 to 8 month period = post-randomization). The S group were taught how to use and integrate the Canadian Diabetes Association's new sugar choices (e.g. added sugar: honey, regular jam, white sugar, etc) into their daily diabetic meal plan. (Abstract shortened by UMI.)

This thesis examined aspects of production and utilization of acetate in humans via measurements of plasma concentrations in different circumstances with particular attention to changes in diabetes. Circulating plasma acetate was measured by a modified acetate kinase-based enzymatic spectrophotometric method with adequate sensitivity and specificity for levels encountered in human plasma. Fasting plasma acetate was increased in diabetics and correlated with glucose and indices of glucose disposal. Levels increased further when they were fed different high- fibre diets. The rise in acetate levels after lactulose ingestion correlated with changing breath hydrogen excretion in subjects with suspected malabsorption. Plasma acetate levels increased during fat infusion, and conversely, fell with suppression of fatty acid levels during euglycaemic clamping. Insulin appeared to promote acetate production from glucose by enhancing glycolysis and acetyl CoA availability, although its activity in reducing lipolysis had an opposite effect. The hepatic formation of acetate from ethanol did not appear influenced by prior chlorpropamide intake. Glucose tolerance was unaffected by a 150mmol/hr acetate load, but acetate tolerance was impaired when glucose was simultaneously available. Adipose tissue lipolysis was suppressed during acetate infusions as evident from reduced levels of glycerol and non-esterifled fatty acids. Blood 'ketone body' levels were increased, suggesting direct conversion from acetate. Possibly as a result, fat oxidation assessed from gaseous exchange, was reduced with infused acetate. Acetate utilization was impaired in diabetic patients from higher fasting plasma levels and slower metabolic clearance. The defect in diabetes was probably due to both over-production and under-utilization, and could be related to the enhanced lipolysis, hyperglycaemia and a reportedly reduced hepatic activity of acetyl CoA synthetase. It was concluded that acetate is derived from both colonic fermentation and endogenous catabolism of glucose and fatty acids and appears rapidly metabolisable in humans. Some areas of further interest in human acetate metabolism were highlighted.

Interactions between manganese (Mn) deficiency and streptozotocin (STZ)-diabetes with respect to tissue antioxidant status were investigated in male, Sprague-Dawley rats. All rats were fed either a Mn-deficient (1 ppm) or a Mn-sufficient (45 ppm) diet for 8 weeks. Diabetes was then induced by tail-vein injection of STZ (60 mg/kg body weight), after which the rats were kept for an additional 4 to 8 weeks. The control groups comprised rats not injected with STZ, which were either Mn-deficient or Mn-sufficient. The Mn-deficient diet decreased the activities of manganese superoxide dismutase (MnSOD) in kidney and heart, and of copper-zinc superoxide dismutase (CuZnSOD) in kidney, in non-diabetic animals. In the diabetic rats, the Mn-deficient diet induced more pronounced decreases in activities of these same enzymes, and also increased liver MnSOD activity. Pancreas weights were significantly lower in Mn-deficient, compared to Mn-sufficient rats. Also, Mn-deficient, diabetic rats were significantly more hyperglycemic in response to a glucose load than Mn-sufficient, suggesting that they may have been more severely diabetic. Surprisingly, plasma and hepatic vitamin E levels increased progressively with the duration of diabetes. Lipid peroxidation, as measured by H₂O₂ -induced production of thiobarbituric acid reactive substances in erythrocytes, plasma lipoperoxides, and renal adipose tissue fluorescence, also increased concomitant with decreased liver and kidney glutathione levels. The effect of vitamin E-deficiency on Mn-deficient, diabetic rats was also investigated. Predictably, vitamin E-deficient rats were almost entirely depleted of plasma and liver vitamin E after 12 weeks on the deficient diets (4 weeks after STZ treatment). Consistent with this, tissue lipid peroxides were elevated compared to vitamin E-sufficient rats. Superimposing vitamin E-deficiency on manganese deficiency failed to add any further deficits in tissue antioxidant status. Higher glycosylated hemoglobin levels were observed in vitamin E-deficient, compared to vitamin E-sufficient, diabetic rats. These findings demonstrate for the first time an interactive effect between manganese deficiency and STZ-diabetes resulting in amplification of tissue antioxidant changes seen with either manganese deficiency or STZ-diabetes alone. This effect of cofactor deprivation in experimental diabetes raises the question of adequacy of the nominally Mn-sufficient diet in insulin-dependent diabetes mellitus. / Land and Food Systems, Faculty of / Graduate