Effects of pure sugar vs. mixed starch fructose loads on food intake

Using a within-subject design, we gave subjects three different 520-530 kcal preloads in the form of puddings in a randomized fashion at weekly intervals. The puddings contained either 50 g of fructose or glucose as the sole carbohydrate source in a protein and fat mixture, or 50 g fructose plus 15 g of starch. Food intake was assessed 2.25 h after the preload was completed. Blood was drawn throughout and assayed for concentrations of glucose and insulin. When the preload contained fructose alone as the sole source of carbohydrate, subjects ate significantly fewer calories and less fat than when the preload contained glucose alone. When starch was added to the fructose preload, there was no significant reduction in calorie and fat intake. Effects on food intake paralleled the rise in plasma insulin levels produced by the different preloads. Implications for use of fructose as an adjunct to weight control efforts are discussed.     

Serum leptin and insulin levels during chronic diurnal fasting

Ramadan fasting is a unique model that is associated with restriction of the timing of food and fluid intake food from dawn to sunset and reduction in meal frequency and sleep duration. Leptin levels are thought to play a role in long-term regulation of caloric intake and fat deposition. However, the long-term changes in leptin levels during this pattern of fasting are not known. The study was conducted on lean (N=6, BMI=22.5+/-0.4) and obese (N=18, BMI=33.1+/-1.0) healthy female volunteers. Fasting serum levels of leptin, insulin and glucose were estimated at baseline (day 1), days 14 and 28 of the month of Ramadan and 2 weeks after Ramadan. Baseline serum levels of leptin were significantly higher in obese (13.5+/-1.96 microg/L,P<0.05) compared with lean subjects (9.60+/-0.80 microg/L) and correlated positively with body fat (r=0.82, P=0.0004). Serum leptin levels exhibited a significant and comparable increase by 39% and 37% throughout the month in lean and obese subjects, respectively. In addition, a significant correlation (r=0.52, P=0.003) was found between changes in serum leptin and serum insulin levels. We conclude that chronic diurnal fasting is associated with significant elevations in serum leptin. These elevations appear to be mediated by changes in serum levels of insulin. These data support the role of insulin in the long-term regulation of leptin secretion during chronic diurnal fasting followed by nocturnal eating during the month of Ramadan.     

Appetite dysfunction in obese males: evidence for role of hyperinsulinaemia in passive overconsumption with a high fat diet

OBJECTIVE: To test the hypothesis that caloric and fat intake in a pre-load meal have no subsequent effects upon blood glucose and insulin concentrations, perceived hunger, subsequent food intake and appetite control in lean and obese men. DESIGN: Lean and obese men reported to the laboratory in the morning in a fasted state where they were subject to an eating test based on the pre-load-test meal paradigm, using a double-blind protocol. The breakfast pre-load was either a reduced caloric low-fat (LF) meal or an overfeeding high-fat (HF) meal. LF was 20% of each individual's average daily energy requirement (ADER) and comprised 60% carbohydrate, 27% protein, and 13% fat, whilst HF was adjusted to yield 55% of the ADER, and comprised 45% carbohydrate, 22% protein and 43% fat. The pre-loads on both trials were administered as one single mean, and were given in a random order. After 5(1/2) h, an ad libitum test-lunch was given to determine how much energy was consumed. Between the two meals, blood samples were collected and subjective hunger ratings were assessed hourly. These variables were measured at 30-min intervals for 75 min after the ad libitum meal. STUDY PARTICIPANTS: Twelve healthy men, six of whom were lean (BMI 22. 50+/-1.08 kg.m2) and six of whom were obese (BMI 39.05+/-11.63 kg. m2) were recruited. RESULTS: When given 55% of their ADER in a HF pre-load meal, the obese group consumed more energy (5426+/-1126 kJ; F1,20=11.45, P<0.01), than the lean group did (3473+/-1114 kJ), accounting for 45% of the ADER in that meal setting. However, no differences between lean and obese intake were noted at the test meal following a LF pre-load. The lean group exhibited a significant inverse correlation (r=0.628, P<0.05) between serum insulin concentration before eating the test meal and the amount of energy consumed at the test meal, while such a relationship was absent in the obese group. CONCLUSION: The obese males were unable to compensate for the caloric overloading when fed a HF (55% ADER) pre-load at a subsequent test meal, whereas a calorically reduced pre-load (20% ADER) produced similar intakes to the lean control group. The inverse relationship noted in the lean group between insulin levels before the test meal and the energy intake at that test meal suggests that insulin may play a role in the regulation of appetite - satiety mechanism in lean males. The absence of such a relationship in the obese may suggest the site for possible appetite dysfunction contributing to obesity. These results further suggest that when obese individuals consume a high-fat meal they are prone to passive overconsumption, whereas lean study participants appear to be more resistant to such a phenomenon.     

Comparative effects of fructose, aspartame, glucose, and water preloads on calorie and macronutrient intake

Using a within-subjects design, we gave over-weight and normal-weight subjects a 500-mL drink of fructose, glucose, or aspartame diluted in lemon-flavored water or plain water in a randomized fashion at about weekly intervals. Food intake was assessed at a buffet lunch that began 38 min after the preload was completed. Blood was drawn throughout and assayed for concentrations of glucose, insulin, glucagon, and free fatty acid. When subjects drank the fructose preload, they subsequently ate fewer overall calories and fewer grams of fat than when they drank any of the other preloads. The aspartame load did not stimulate intake beyond the plain-water control. The effects of the oxidation of fructose as a possible mechanism for the reduction in food intake is discussed. The effects of insulin in stimulating intake are also discussed.     

Caloric intake and hypothalamic neurotransmitters in Zucker rats made acutely diabetic with streptozocin

Zucker rats, lean and obese, treated with low dose intraperitoneal injections of streptozocin become hyperglycemic within 24h. Insulin levels fall, although the obese animal remains hyperinsulinemic. Associated with these changes in glucose and insulin there are transient decreases in caloric intake. Macronutrient selection studies show that protein consumption decreases. There is a trend for fat intake to decrease. The levels of hypothalamic neurotransmitters in the lean animals are not altered by streptozocin. The levels of 5-hydroxyindoleacetic acid increases in the streptozocin-treated obese animal in the paraventricular region, ventromedial region and the raphe. Serotonin is also significantly increased in the paraventricular region of the obese rat. These results suggest that acutely, treatment with streptozocin injures pancreatic islets, causing, in turn, decreases in insulin levels so that hyperglycemia ensues in both phenotypes. Associated with these perturbations are decreases in caloric intake. The magnitude of change in insulin levels is much greater in the obese rat. It is hypothesized that in the obese Zucker rat decrements in food intake are mediated by increase in serotonin turnover in the hypothalamus and these changes are related to changes of insulin levels. These data support the concept that circulating insulin affects hypothalamic neurotransmitters.     

Response of adult lean and obese female Zucker rats to food restriction and refeeding

Lean and obese female Zucker rats were either fed ad libitum (ad libitum-fed lean and ad libitum-fed obese), food-restricted (restricted lean and restricted obese) at 50% of ad libitum intake for 3 weeks from 19–20 weeks of age, or food-restricted and then refed ad libitum for 1 week (restricted-refed lean and restricted-refed obese). Following food restriction, body weights of restricted rats were significantly lower than ad libitum-fed rats within genotype. Body weights of restricted-refed rats were not different from either ad libitum-fed or restricted rats within genotype. Restricted-refed lean rats returned to their previous ad libitum food intake, whereas restricted-refed obese rats ate significantly more food. Both restricted and restricted-refed lean rats had lowered serum insulin levels compared to ad libitum-fed lean rats, whereas there was no effect on serum insulin levels in obese rats. Liver weights and hepatocyte conversion of glucose to fatty acids, glyceride-glycerol and CO₂ were not affected by food restriction or refeeding in lean rats. Among obese rats, restricted obese rats had the smallest liver weights, and restricted-refed obese rats had the highest. Restricted-refed obese rats had greater rates of hepatic glucose metabolism compared to all other groups. Ad libitum-fed lean and restricted-refed lean rats had similar fat pad weights that were significantly greater than those of restricted lean rats. Dietary intervention had no effect on fat pad weight in obese rats. There was no effect of food restriction or refeeding on adipocyte glucose metabolism except for higher glucose conversion to CO₂ for restricted lean rats in comparison to values for all other groups. These results demonstrate that body weight changes of adult female obese rats in response to food restriction and refeeding are similar to those of lean rats; but the effects of liver and adipose tissue weights are different.     

Caloric Intake and Hypothalamic Neurotransmitters in Zucker Rats made Acutely Diabetic with Streptozocin

Abstract

Zucker rats, lean and obese, treated with low dose intraperitoneal injections of streptozocin become hyperglycemic within 24 h. Insulin levels fall, although the obese animal remains hyperinsulinemic. Associated with these changes in glucose and insulin there are transient decreases in caloric intake. Macronutrient selection studies show that protein consumption decreases. There is a trend for fat intake to decrease. The levels of hypothalamic neurotransmitters in the lean animals are not altered by streptozocin. The levels of 5-hydroxyindoleacetic acid increases in the streptozocin-treated obese animal in the paraventricular region, ventromedial region and the raphe. Serotonin is also significantly increased in the paraventricular region of the obese rat. These results suggest that acutely, treatment with streptozocin injures pancreatic islets, causing, in turn, decreases in insulin levels so that hyperglycemia ensues in both phenotypes. Associated with these perturbations are decreases in caloric intake. The magnitude of change in insulin levels is much greater in the obese rat. It is hypothesized that in the obese Zucker rat decrements in food intake are mediated by increase in serotonin turnover in the hypothalamus and these changes are related to changes of insulin levels. These data support the concept that circulating insulin affects hypothalamic neurotransmitters.     

Delayed Onset of Ataxia in a Patient with Short Bowel Syndrome: A Case of Vitamin E Deficiency

Lean and obese Zucker rats were deprived of food for 12, 24, and 48 h. After sacrifice, plasma and brain tissue were saved for hormone and regional hypothalamic monoamine analysis. An ad libitum group was killed at time 0 for comparison to the food deprived groups. Insulin (I), C-peptide (CP), glucose, and the CP/I ratio were dramatically different across phenotype. Glucagon was only different at 12 h of caloric deprivation. Insulin secretion dropped substantially with fasting as reflected by the decrease in C-peptide plasma levels in both lean and obese rats. The CP/I ratio, which indicates clearance of insulin, increased in lean rats across time of fasting but did not significantly change in obese rats. Several distinct changes occurred between phenotypes in the hypothalamus across food deprivation. Lateral hypothalamic 5HT content and 5HT turnover (5HIAA/5HT) increased in lean but not obese rats during the period of fasting. Likewise ventromedial hypothalamic dopamine turnover (NE/DA) decreased during caloric deprivation in lean rats but not in the obese rats. This same turnover was increased in the PVNA of obese but not lean rats during caloric deprivation. Individual measurements of both C-peptide and insulin correlated significantly with LH 5HT turnover and VMH dopamine turnover in lean rats but not obese rats. These data suggest that obese rat's hypothalami may possibly be insensitive to insulin or some factor such as leptin that insulin may regulate. Because obese rats cannot change their levels of hypothalamic neurotransmitters when insulin or some other insulin induced factor changes, may suggest clues as to why these rats became obese. Perhaps these data may help explain the altered body weight set-point, increased adiposity, and hyperphagia in these animals.     

Variability of blood glucose and plasma insulin responses after replacing ham by egg in the breakfast of obese subjects

The effects of replacing ham protein by egg protein was tested in eleven obese subjects during two isocaloric breakfasts. Blood glucose (BG) and plasma insulin (IRI) responses were measured during four hours. The replacement of ham by egg significantly decreased blood glucose levels in all subjects. However, the variability of the responses led us to divide the obese subjects into two subgroups. In five subjects (E group), the replacement of ham by egg produced a significant decrease in blood glucose and plasma insulin responses (BG: from 7.71±0.50 to 6.66±0.61 mmol/l at 30 minutes; IRI: from 148±23 to 76±12 μU/ml at 50 minutes). No effect was observed in the other six subjects (N.E. group) apart from an increase in BG from 6.55±0.50 to 7.55±0.55 mmol/l at 65 minutes. Among the known parameters of the study, the postprandial decrease in blood glucose levels observed after egg intake in some obese subjects seemed to be related, to the usual caloric intake of the subjects before the experiment. The usual caloric intake and the detailed composition of meals must therefore be given when metabolic studies on glucose tolerance are carried out in obese subjects.     

Is fiber satiating? Effects of a high fiber preload on subsequent food intake of normal-weight and obese young men

This study was designed to test whether a high fiber preload can suppress food intake at a subsequent test meal. Fifty male undergraduates, 31 of normal body weight and 19 at least 15 per cent overweight, participated as paid volunteers. So as not to inhibit spontaneous food intake, they were told that the investigators were studying the effects of the parasympathetic nervous system on cognitive processes and they were given a picture rating task to perform. The stated rationale for having the subjects eat the preload between two sets of pictures was to alter the state of parasympathetic activation. The preload consisted of two roast beef sandwich halves containing a total of 400 kcal and either 5.2 or 0.2 g of crude fiber in the bread. The preload was eaten by the subjects, their meal was intentionally interrupted and then they were allowed to finish eating 30-45 minutes later (test meal). Obese subjects ate significantly fewer sandwich halves after the high than after the low fiber preload. Obese subjects ate significantly more than non-obese subjects in the low fiber treatment so that the effect of the high fiber was to normalize their intake. Although both obese and normal-weight subjects reported feeling fuller after the high fiber preload, the non-obese subjects ate virtually the same amount in both treatments. Obese subjects reported liking the high fiber bread less well than the low fiber bread but additional statistical analyses showed an intake-suppressing effect of fiber even after controlling for bread rating. These results support the hypothesis that fiber reduces caloric intake in obese people.     

Food intake of very obese persons: quantitative and qualitative aspects.

To document the caloric intake of very obese persons and investigate the food choices and dietary composition that maintain severe obesity, we studied the self-selected food intake required to maintain stable weight in two groups of very obese subjects: 11 inpatients with a mean weight 181% above desirable body weight and 35 outpatients with a mean weight 125% above desirable body weight. Qualitative and quantitative food intake were evaluated using records obtained on the hospital metabolic ward for the inpatients and using self-recorded food records for the outpatients. Absolute caloric intake in both groups was greater in proportion to the degree of obesity (deviation from desirable body weight); caloric intake per unit of lean body mass (kilocalories per gram urinary creatinine) was constant regardless of the degree of obesity and was essentially the same as that of normal nonobese persons. Food records indicated that the obese subjects maintained their high caloric intake by consuming mostly foods of high caloric density, with occasional binge eating. They largely avoided foods of low intrinsic energy density and modified-calorie foods, ie, foods with decreased fat, nonnutritive sweeteners, or fillers. By substituting foods of lower caloric density for usual food choices from the same food group, obese persons could decrease caloric intake by 20% and increase potential for notable weight loss.     

Catalytic amounts of fructose may improve glucose tolerance in subjects with uncontrolled non-insulin-dependent diabetes

BACKGROUND: It was suggested that acute ingestion of small amounts of fructose can improve glucose homeostasis. AIM: To study the effect of a long-term tri-daily supplementation of catalytic amounts of fructose on glucose tolerance of subjects with type 2 diabetes (NIDDM). METHODS: A double-blind, placebo-controlled study. Twenty-six subjects with uncontrolled NIDDM as indicated by high levels of hemoglobin A1C (Hgb(A1c)) and 2-h postprandial glucose levels >200 mg% were assigned to either fructose or maltodextrin supplementation (7.5 g) tri-daily after each main meal. The subjects were challenged with a fixed meal and blood was drawn for determining levels of glucose, insulin and triglycerides before and 2 h after meal at baseline and 1 month after study entry. Blood was drawn for total cholesterol, high-density and low-density lipoprotein cholesterol (LDL-c), fructosamine and Hgb(A1C) before study entry and at 1, 2 and 3 months into the study. RESULTS: No changes were observed in the difference between postprandial and pre-meal glucose, insulin or triglyceride levels in each group or between groups. No significant statistical differences were found in weight, total cholesterol, LDL-c and high-density lipoprotein cholesterol (HDL-c) in each group or between groups along the study period. After 1 month fructosamin levels decreased in the fructose-supplemented group but not in the maltodextrin-supplemented group (P<0.052). Hgb(A1C) levels decreased with time in both groups but were significantly lower at 2 months in the fructose group as compared to the maltodextrin group (P<0.03). CONCLUSIONS: Subjects with NIDDM may benefit from daily supplementation of catalytic amounts of fructose in their diet.     

The ability of habitual exercise to influence appetite and food intake in response to high- and low-energy preloads in man

The present study tested the hypothesis that habitual exercisers demonstrate an increased accuracy of regulation of food intake in compensation for previous dietary energy intake. Twenty-three lean healthy male subjects were divided into two groups on the basis of their habitual exercise levels: non-exercisers (no exercise sessions/week, n 9), and exercisers (>two exercise sessions of 40 min or more/week, n 14). The appetite response to covert liquid preloads of high (2513 kJ) energy (HE) and low (1008 kJ) energy (LE) was investigated Sixty minutes after the preload subjects were offered an ab libitum buffet-style meal and energy intake (EI) was calculated. Subjective hunger and satiety were assessed throughout using self-rated visual-analogue scales. Buffet EI in non-exercisers was not significantly different following the LE or HE preloads (mean compensation 7 %), but the exercise group significantly reduced their energy intake following the HE, compared with the LE, preload (mean compensation 90 %; P=0.0035). A broadly similar pattern of response was observed for both moderate (two to three sessions/week, n 7) and high exercisers (>four sessions/week, n 7). There were no significant differences between hunger or satiety ratings following HE or LE preloads for either group. However non-exercisers scored significantly higher on their self-ratings of hunger at the start of the study, before preload consumption, compared with the exercisers (P<0.01). These findings demonstrate that habitual exercisers have an increased accuracy of short-term regulation of food intake in compensation for preload manipulation, and provide additional support for advocating regular exercise in the prevention of overweight and obesity.     

Effects of fructose feeding on lipid parameters in obese and lean, diabetic and nondiabetic Zucker rats

Effects of fructose feeding in moderate amounts on lipid metabolism of obese versus lean, and diabetic versus nondiabetic Zucker rats, were studied. Forty pairs of male lean and obese animals were assigned to two dietary groups, fructose and glucose. For each diet, one-half of lean and obese animals were injected with streptozotocin intraperitoneally (i.p.) to induce diabetes, and the other half were injected with buffer i.p. as a nondiabetic control group. After 9 wk of feeding, animals were fasted overnight, decapitated and exsanguinated. Organs were removed and weighed. Blood glucose, insulin, lactic acid, triglycerides, cholesterol, total liver lipids and urinary glucose were determined. Hyperphagia was observed in obese, non-diabetic and lean-diabetic animals. Streptozotocin injection drastically reduced insulin levels, and produced an impairment of growth, hyperglycemia, glucosuria, polydipsia and polyuria. Fructose feeding increased organ weights in kidney, liver and retroperitoneal adipose tissue, regardless of diabetic state. However, lactic acid levels were lower in fructose-fed groups than glucose-fed groups. In obese rats serum triglyceride levels were also lower in fructose-fed groups than in glucose-fed groups. Serum cholesterol was not affected by fructose feeding. The results indicated that fructose feeding did not produce hyperlipemia and lactic acidosis in the blood circulation in Zucker rats. However, fructose feeding did not improve glucose intolerance in diabetic animals, rather fructose feeding produced hyperinsulinemia in nondiabetic, obese animals.     

No decrease in free IGF-I with increasing insulin in obesity-related insulin resistance

OBJECTIVE: Different facts suggest that the insulin growth factor (IGF)/ insulin growth factor-binding protein (IGFBP) system may be regulated by factors other than growth hormone. It has been proposed that, in healthy subjects, free IGF-I plays a role in glucose metabolism. The role of free IGF-I in glucose homeostasis in insulin resistance is poorly understood. This study was undertaken to evaluate the effects of acute changes in plasma glucose and insulin levels on free IGF-I and IGFBP-1 in obese and non-obese subjects. RESEARCH METHODS AND PROCEDURES: Nineteen lean and 24 obese subjects were investigated. A frequently sampled intravenous glucose tolerance test was performed. Free IGF-I and IGFBP-1 were determined at 0, 19, 22, 50, 100, and 180 minutes. RESULTS: Basal free IGF-I levels tended to be higher and IGFBP-1 lower in obese than in lean subjects. IGFBP-1 levels inversely correlated with basal insulin concentration. To determine the effects of insulin on the availability of free IGF-I and IGFBP-1, changes in their plasma concentrations were measured during a frequently sampled intravenous glucose tolerance test. After insulin administration, a significant suppression of free IGF-I at 22% was observed in lean subjects. In contrast, plasma-free IGF-I levels remained essentially unchanged in the obese group. The differences between both groups were statistically significant at 100 minutes (p < 0.01) and 180 minutes (p < 0.05). Serum IGFBP-1 was suppressed to a similar extent in both groups. DISCUSSION: These data suggest that the concentrations of free IGF-I and IGFBP-1 are differentially regulated by obesity. Obesity-related insulin resistance leads to unsuppressed free IGF-I levels.     

Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity

Obesity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged > or = 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d. The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.     

Effects of a fat substitute, sucrose polyester, on food intake, body composition, and serum factors in lean and obese Zucker rats

Sucrose polyester, a fat substitute, has shown promise in reducing blood cholesterol and body weight of obese individuals. Effects of this compound in the Zucker rat, a genetic model of obesity, are unknown. Thus, we examined food intake, body weight, body composition, and several metabolic parameters in sera of lean and obese female Zucker rats. Eight-week-old lean and obese animals were given a choice between a control diet (15% corn oil) and fat substitute diet (5% corn oil and 10% sucrose polyester) for 2 days. Next, one-half of the lean and obese groups received control diet; the remaining lean and obese rats received fat substitute diet for 18 days. Cumulative food intake was depressed in fat substitute groups relative to control-fed animals; however, this effect was more predominant in obese animals. Obese rats consuming fat substitute diet (O-FS) gained less weight as compared to obese control-fed animals (O-C). Lean rats given fat substitute (L-FS) did not have significantly different body weights as compared to the L-C group. Fat substitute groups, combined, had lower body fat and higher body water as compared to controls. The O-FS group had lower serum glucose and insulin and higher fatty acid levels compared to the O-C group. There were no differences in serum cholesterol, HDL, or triglyceride levels due to fat substitute diet. These data suggest that the obese Zucker rat is unable to defend its body weight when dietary fat is replaced with sucrose polyester.     

Hunger and food intake following consumption of low-calorie foods

Although high-intensity sweeteners are widely used to decrease the energy density of foods, little is known about how this affects hunger and food intake. We have studied the effects of consumption of commercially available foods sweetened with either sucrose or aspartame on subjective appetite ratings and food intake. When normal-weight non-dieting males and females were given large portions of either a high- or low-calorie pudding or jello and instructed to eat as much as they liked, they ate similar weights of the different caloric versions of each food. Despite the resulting difference in caloric intake (up to 206 kcal), subjects showed only a non-significant trend towards caloric compensation when presented with a variety of foods 2 h later. Total caloric intake (preload plus test meal) did not differ between conditions. Ratings of hunger, desire to eat, the amount subjects wanted to eat, and the pleasantness of the taste of the eaten food were similarly decreased and fullness similarly increased by consumption of the different caloric versions of the foods. Awareness of the caloric content of the foods did not influence intake or appetite in that both informed and uniformed subjects responded similarly in the tests. Thus reduced calorie foods suppressed ratings of hunger for several hours after consumption, but were not associated with a significant reduction in total energy intake.     

Hypocaloric diets and ketogenesis in the management of obese gestational diabetic women.

The extent to which given levels of caloric restriction will improve glycemic status but increase plasma ketone bodies in gestational diabetic women has received little attention. After reviewing the underlying physiology, we present data on two feeding studies investigating the question. In the first, a weight-maintaining approximately 2400-kcal/day diet was fed on a metabolic ward to 12 gestational diabetic women for 1 week. In the second week, subjects were randomized to a continuation of the 2400-kcal/day diet or to a 1200-kcal/day diet. Twenty-four-hour mean glucose levels remained unchanged in the control group but declined in the calorie-restricted group (6.7 mM or 121 mg/dl in week 1 vs 5.4 mM or 97.3 mg/dl in week 2) (p less than 0.01). Nine-hour overnight fasting plasma insulin also declined but oral glucose tolerance did not improve with caloric restriction. Fasting plasma beta-hydroxybutyrate rose in the calorie-restricted group, along with an increase in ketonuria, but not in the control group. A second study compared the impact of a 33% calorie-restricted diet or insulin to a full-calorie diet in a similar 2-week experimental design and measured hepatic glucose output and insulin sensitivity with dideuterated glucose before and during an insulin clamp. Diet in three subjects improved fasting and 24-hr mean glucose by 22 and 10%, respectively, whereas prophylactic insulin in three subjects produced 0 and 4% reductions, respectively. On average, ketonuria after a 9-hr fast declined to an equivalent degree with both treatments. Hepatic glucose output and insulin sensitivity were not statistically significantly altered by gestational diabetes or the therapeutic interventions compared to nondiabetic normal weight or obese pregnant controls. In conclusion, 50% caloric restriction improves glycemic status in obese women with gestational diabetes but is associated with an increase in ketonuria, which is of uncertain significance. An intermediate 33% level of caloric restriction (to 1600-1800 kcal daily) may be more appropriate in dietary management of obese woman with gestational diabetes mellitus and more effective than prophylactic insulin. Further studies are required to confirm these findings.     

Hypocaloric diets and ketogenesis in the management of obese gestational diabetic women.

The extent to which given levels of caloric restriction will improve glycemic status but increase plasma ketone bodies in gestational diabetic women has received little attention. After reviewing the underlying physiology, we present data on two feeding studies investigating the question. In the first, a weight-maintaining approximately 2400-kcal/day diet was fed on a metabolic ward to 12 gestational diabetic women for 1 week. In the second week, subjects were randomized to a continuation of the 2400-kcal/day diet or to a 1200-kcal/day diet. Twenty-four-hour mean glucose levels remained unchanged in the control group but declined in the calorie-restricted group (6.7 mM or 121 mg/dl in week 1 vs 5.4 mM or 97.3 mg/dl in week 2) (p less than 0.01). Nine-hour overnight fasting plasma insulin also declined but oral glucose tolerance did not improve with caloric restriction. Fasting plasma beta-hydroxybutyrate rose in the calorie-restricted group, along with an increase in ketonuria, but not in the control group. A second study compared the impact of a 33% calorie-restricted diet or insulin to a full-calorie diet in a similar 2-week experimental design and measured hepatic glucose output and insulin sensitivity with dideuterated glucose before and during an insulin clamp. Diet in three subjects improved fasting and 24-hr mean glucose by 22 and 10%, respectively, whereas prophylactic insulin in three subjects produced 0 and 4% reductions, respectively. On average, ketonuria after a 9-hr fast declined to an equivalent degree with both treatments. Hepatic glucose output and insulin sensitivity were not statistically significantly altered by gestational diabetes or the therapeutic interventions compared to nondiabetic normal weight or obese pregnant controls. In conclusion, 50% caloric restriction improves glycemic status in obese women with gestational diabetes but is associated with an increase in ketonuria, which is of uncertain significance. An intermediate 33% level of caloric restriction (to 1600-1800 kcal daily) may be more appropriate in dietary management of obese woman with gestational diabetes mellitus and more effective than prophylactic insulin. Further studies are required to confirm these findings.