Joyce E. Swanson

Metabolic Effects of Dietary Fructose in Diabetic Subjects

OBJECTIVE To assess the metabolic effects of chronic dietary fructose consumption in diabetic subjects. RESEARCH DESIGN AND METHODS Six type I and 12 type II diabetic subjects consumed, in random order, two isocaloric study diets for 28 days. In one diet, 20% of energy was derived from fructose. In the other diet, <3% of energy came from fructose, and carbohydrate energy was derived primarily from starch. Both study diets were composed of common foods. All meals were prepared in a metabolic kitchen where all foods were weighed during meal preparation. RESULTS Mean plasma glucose, urine glucose, and serum glycosylated albumin values were lower during the fructose diet than during the starch diet, but the differences achieved only marginal statistical significance. The day-28 value for mean plasma glucose was 12.5% lower (P = 0.03) during the fructose diet than during the starch diet. At days 14, 21, and 28, fasting serum cholesterol and LDL cholesterol were both significantly higher during the fructose diet than during the starch diet. The day-28 values for serum cholesterol and LDL cholesterol during the fructose diet were 6.9% (P = 0.008) and 10.9% (P = 0.002) higher, respectively, than the corresponding values during the starch diet. No differences were observed between the study diets in fasting serum HDL cholesterol, fasting serum triglycerides, peak postprandial serum triglycerides, or fasting serum lactate. Peak postprandial serum lactate was significantly higher during the fructose diet. Type I and type II diabetic subjects responded to the diets in a consistent way, but type I subjects experienced significantly more hypoglycemia during the fructose diet than during the starch diet. CONCLUSIONS A high-fructose diet may result in reduced glycemia in diabetic subjects but at the expense of increased fasting serum total and LDL cholesterol.

Metabolic Effects of Dietary Sucrose in Type II Diabetic Subjects

Objective— To assess in diabetic subjects the effects of dietary sucrose on glycemia and lipemia. Research Design and Methods— Twelve type II diabetic subjects consumed, in random order, two isocaloric, 55% carbohydrate study diets for 28 days. In one diet, 19% of energy was derived from sucrose. In the other diet, <3% of energy was derived from sucrose, and carbohydrate energy came primarily from starch. Both study diets were composed of common foods. All meals were prepared in a metabolic kitchen where foods were weighed during meal preparation. Results— No significant differences were noted between the study diets at any time point in mean plasma glucose. At day 28, mean plasma glucose values for the sucrose diet were 9.6 ± 0.5 mM and for the starch diet were 9.4 ± 0.6 mM (P = 0.63). Also, no significant differences were observed between the study diets in urine glucose, fasting serum total, HDL, or LDL cholesterol; fasting serum TG; or peak postprandial serum TG. Conclusions— A high sucrose diet did not adversely affect glycemia or lipemia in type II diabetic subjects.

Chronic treatment with phentermine combined with fenfluramine lowers plasma serotonin

As expected on the basis of published research in both humans and animals, treatment with phentermine/fenfluramine lowers plasma 5-hydroxytryptamine [corrected], whereas treatment with phentermine had no significant effect. In light of these findings, future research should focus on mechanisms other than increased plasma 5-hydroxytryptamine [corrected] to explain how fenfluramine increases the risk of primary pulmonary hypertension and valvular heart disease.

Energy and Macronutrient Intake of Type 2 Diabetics Participating in a Clinical Trial of Pharmacologic Induction of Weight Loss

Abstract Forty-four overweight subjects with type 2 diabetes mellitus were enrolled in a randomized, placebo-controlled, double blind trial of pharmacologic induction of weight loss. All subjects received intensive nutrition counseling, an exercise prescription, instruction on behavioral management, and were randomly assigned to fenfluramine 20mg three times daily and phentermine 37.5mg daily (n=23) or dual placebos (n=21). Drug therapy continued until September 1997 when fenfluramine was withdrawn from the US market. Dietary intake was assessed by administration of a food frequency questionnaire (Block 95) at baseline, 2, 6, and 12 months. Mean ± SEM baseline data for the placebo group and the active drug group, respectively, were: Weight (kg) 106 ± 4, 108 ± 4; kilocalories 2991 ± 445, 3053 ± 482; carbohydrate (%) 36.9 ± 1.5, 40.2 ± 2.5; protein (%) 15.8 ± 1.9, 14.8 ± 1.1; fat (%) 47.8 ± 2.6, 44.7 ± 2.5. Changes from baseline (* placebo vs. active, p * −491±1833.1±1.31.0±0.8−4.2±1.56 MonthsPlacebo (n=13)−2.7±1.4−636±2415.2±1.70.6±0.8−6.2±1.6Active (n=13)−9.6±1.5 * −284±2774.6±2.8−0.3±0.7−4.5±2.612 MonthsPlacebo (n=8)−2.5±2.5−670±3104.2±2.1−0.1±1.4−4.8±2.0Active (n=8)−8.1±1.6−605±277−3.4±5.14.5±3.3−4.6±4.5 Body weight was reduced at all time points for both groups, but was significantly reduced in the drug treatment groups at 2 and 6 months. Although a reduction in reported total energy intake was observed in both groups, no significant difference was detectable between groups. The reported change in intake was accounted for primarily by a reduction in fat intake.

Energy Expenditure and Body Composition of Type 2 Diabetics Participating in a Clinical Trial of Pharmacologic Induction of Weight Loss

Abstract Forty-four overweight subjects with type 2 diabetes mellitus were enrolled in a randomized, placebo-controlled, double blind trial of pharmacologic induction of weight loss. All subjects received intensive nutrition counseling, an exercise prescription, instruction on behavioral management, and were randomly assigned to fenfluramine 20mg three times daily and phentermine 37.5mg daily (n=23) or dual placebos (n=21). Drug therapy continued until September 1997 when fenfluramine was withdrawn from the US market. Body fat composition was assessed by skinfold measurement. Resting energy expenditure was measured with a DeltaTrac metabolic monitor. Physical activity was assessed by questionnaire. Mean ± SEM baseline data for the placebo group and the active drug group, respectively, were: Weight (kg) 106 ± 4, 108 ± 4; BMI (kg/m 2 ) 37.7 ± 1.4, 38.5 ± 2.4; Body Fat (%) 39.1 ± 1.7,40.0 ± 2.3; REE (kcal) 2180 ± 73, 2087 ± 173; and weekly energy expenditure in physical activity (PA, kcal) 1410 ± 613, 1267 ± 367. The changes from baseline were as follows (placebo vs. active, **p 2 )(%)(kcal)(kcal)Placebo (n=18)−1.6±0.5−0.5±0.2−0.5±0.5−13±43344±274Active (n=21)−7.9±1.2**−2.5±0.4**−3.0±0.7**−265±41**938±2896 MonthsPlacebo (n=13)−2.7±1.4−0.8±0.5−0.7±0.7−130±521349±503Active (n=13)−9.6±1.5**−3.2±0.5**−2.5±1.0−262±6260±466*12 MonthsPlacebo (n=8)−2.5±2.5−0.6±0.81.5±1.4−51±491408±546Active (n=8)−8.1±1.6*−2.6±0.7*−1.8±0.9*−139±27650±319 The observed reduction in both body weight and BMI were both statistically significant at 2 and 6 months and approaching significance at 12 months in the active group. As expected, the reduction in body weight was accompanied by a reduction in REE and in percentage of body fat.