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A two year old dystrophic boy with chronic diarrhea was described. At the age of 6 month the boy developed a severe gastroenteritis with a secundary lactase deficiency. Dietary treatment was however not successful and consequently the boy became dystrophic. At last, an abuse of sweetener was diagnosed.
The effects of fructose loading on the integrated cardiovascular function in vivo, glycemic control, glucose tolerance, and plasma lipid levels in nondiabetic and streptozotocin (STZ) diabetic rats were investigated. Endothelial morphology of the thoracic aorta was also assessed with scanning electron microscopy. Fructose-loaded nondiabetic rats exhibited elevated blood pressure and pulse rate, and signs of arterial atherogenesis, such as focal adherence of leukocytes and fibrin to the endothelium. Intraperitoneal glucose tolerance tests revealed a greater increase in plasma insulin in response to glucose challenge in these animals than in the control. Compared with the untreated STZ-diabetic animals, fructose-loaded diabetic rats had significantly greater hyperglycemia, glucose intolerance, and hyperlipidemia and higher blood pressure, but had a similar degree of hypoinsulinemia, cardiac dysfunction, and cardiac enlargement. They also showed signs of early atherogenesis. The central venous pressure and the susceptibilities of the rats to the induction of ventricular arrhythmias by intravenous infusion of aconitine were not significantly affected by either STZ injection or fructose loading. It is concluded that prolonged intake of an excessive amount of fructose has detrimental effects on the cardiovascular system, glucose metabolism, and plasma lipid levels in both nondiabetic and STZ-diabetic rats.
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Following ion-exchange chromatography and subsequent thin-layer chromatography, 3 peculiar oligosaccharide excretion patterns were distinguished in 3 patients with beta-galactosidase deficiency. Each patient differed clinically and it is proposed that this method may be of use in characterizing various forms of beta-galactosidase deficiency.
BACKGROUND: Fructose malabsorption is frequently seen in the general population and is characterised by the inability to absorb fructose efficiently. Due to fructose malabsorption, fructose reaches the colon where it is broken down by bacteria to short fatty acids, CO(2) and H(2). Bloating, cramps, osmotic diarrhea and other symptoms of irritable bowel syndrome are the consequence. We recently found that fructose malabsorption is associated with low plasma folic acid concentrations and low serum tryptophan and zinc. Because fructose malabsorption apparently is associated not only with malabsorption of other nutrients, but also with abdominal discomfort, it was of interest to examine whether mild pancreatitis may be involved. METHODS: We retrospectively examined our data in 159 otherwise healthy adults (110 females, 49 males) aged 14-84 years (mean 45.6+/-14.4 S.D.) with gastrointestinal complaints for serum amylase and serum lipase concentrations. The patients have been tested earlier for fructose malabsorption and lactose maldigestion by measuring breath H(2) concentrations after an oral dose of 25 g fructose and 50 g lactose, respectively, 1 week apart. RESULTS: Fructose malabsorption (H(2) concentrations > or =20 ppm over baseline values) was detected in 107 of 159 individuals (67.3%). These subjects with fructose malabsorption presented with significantly higher serum amylase concentrations (73.1 U/l+/-25.7 S.D.) compared to individuals with normal fructose absorption (59.6 U/l+17.9 S.D; p=0.0009). Fructose malabsorbers also presented with higher serum lipase concentrations (122.0 U/l+/-100.3 S.D.) compared to normals (89.5 U/l+/-46.5 S.D.; p<0.05). To determine whether this finding is a consequence of any sort of malabsorption syndrome or whether it is specific for fructose malabsorption, all subjects were screened for lactose maldigestion. Lactose maldigestion (H(2) concentrations>20 ppm over baseline after lactose loading) was found in 50 of 159 individuals (31.4%). There were no significant differences in either amylase or lipase concentrations in lactose maldigestors. CONCLUSION: Serum amylase and lipase concentrations are higher in subjects with fructose malabsorption compared to normals. Therefore, fructose malabsorption should be considered as a differential diagnosis in moderately elevated serum amylase.
It remains unclear whether adiposity plays an important role in glucose intolerance independently of insulin resistance. We investigated whether adiposity and insulin resistance had distinct roles in glucose intolerance in rats. We examined glucose tolerance and insulin resistance using ventromedial hypothalamic (VMH)-lesioned rats in the dynamic and the static phases of obesity (2 and 14 weeks after lesioning, respectively). Rats were fed either normal chow or a fructose-enriched diet (60% of total calories). The intravenous glucose tolerance test (IVGTT) was performed by bolus injection of glucose solution (1 g/kg) and blood sampling after 0, 5 10, 30, and 60 minutes. Insulin resistance was evaluated from the steady-state plasma glucose (SSPG) value during continuous infusion of glucose, insulin, and somatostatin. SSPG was not increased in VMH-lesioned rats in the dynamic phase of obesity, but increased markedly in the static phase. The area under the glucose curve (glucose AUC) during IVGTT was increased in VMH-lesioned rats in the static phase, but not in the dynamic phase, when compared with their sham-operated counterparts. A fructose-enriched diet for 2 or 14 weeks increased SSPG values to a similar extent in both sham-operated and VMH-lesioned rats without inducing excess adiposity, but glucose intolerance was only developed in the obese rats. The plasma leptin level, an excellent indicator of adiposity, was significantly related to the glucose AUC independently of the insulin level. Insulin resistance or increased adiposity alone is not sufficient to impair glucose tolerance, but increased adiposity plays an important role in the development of glucose intolerance in an insulin-resistant state.
Sugar intolerance is a common problem in paediatric practice. The usual type is lactose intolerance following gastroenteritis, but it may also occur in a wide variety of disorders of the small bowel. Diagnosis depends upon identification of reducing substances in the stools. An approach to dietary management of lactose intolerance is given and use of a carbohydrate-free formula in secondary monosaccharide intolerance is described. In each situation, threshold for digestion or absorbtion of carbohydrate is approached gradually from below, and overflow detected by Clinitest stool testing.
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High-fructose consumption is associated with insulin resistance and diabetic dyslipidemia, but the underlying mechanism is unclear. We show in hamsters that high-fructose feeding stimulated forkhead box O1 (FoxO1) production and promoted its nuclear redistribution in liver, correlating with augmented apolipoprotein C-III (apoC-III) production and impaired triglyceride metabolism. High-fructose feeding upregulated peroxisome proliferator-activated receptor-gamma coactivator-1beta and sterol regulatory element binding protein-1c expression, accounting for increased fat infiltration in liver. High-fructose-fed hamsters developed hypertriglyceridemia, accompanied by hyperinsulinemia and glucose intolerance. These metabolic aberrations were reversible by fenofibrate, a commonly used anti-hypertriglyceridemia agent that is known to bind and activate peroxisome proliferator-activated receptor-alpha (PPARalpha). PPARalpha physically interacted with, but functionally antagonized, FoxO1 in hepatic apoC-III expression. These data underscore the importance of FoxO1 deregulation in the pathogenesis of hypertriglyceridemia in high-fructose-fed hamsters. Counterregulation of hepatic FoxO1 activity by PPARalpha constitutes an important mechanism by which fibrates act to curb apoC-III overproduction and ameliorate hypertriglyceridemia.
We examined the effects of the potassium channel opener KRN4884 (5-amino-N-[2-(2-chlorophenyl)ethyl]-N'-cyano-3-pyridinecarboxamidine ) on cardiovascular metabolic syndrome (i.e., syndrome X), in rats. High-fructose diet rats developed hypertension, hypertriglyceridemia, increased total cholesterol/HDL (high-density lipoprotein)-cholesterol ratio, and hyperinsulinemia, KRN4884 (0.3-3.0 mg/kg, twice a day for 14 days, p.o.) alleviated the risk factors in fructose-fed rats. Furthermore, fructose-fed rats exhibited impairment of glucose tolerance and excess insulin secretion when loaded with glucose orally. Treatment with KRN4884 (1.0 mg/kg, twice a day for 14 days, p.o.) improved the glucose intolerance and inhibited hypersecretion of insulin in the glucose-loaded, fructose-fed rats. In contrast, KRN4884 (0.3-1.0 mg/kg, twice a day for 10 days, p.o.) did not affect serum triglyceride, cholesterol, glucose, or insulin concentrations in normal rats. LPL (lipoprotein lipase) activities in skeletal muscle and adipose tissue, and HTGL (hepatic triglyceride lipase) activity in liver were measured after administration of KRN4884 or vehicle twice a day for 14 days in fructose-fed rats. KRN4884 caused a significant increase in LPL activity in muscle and tended to increase LPL activity in adipose tissue in fructose-fed rats. HTGL was decreased in fructose-fed rats as compared with normal controls and was unaffected by KRN4884. These findings suggested that KRN4884 enhances insulin sensitivity and LPL activity, which are related to glucose and lipid metabolism and may be useful for the treatment of syndrome X.
The intestinal brush-border enzyme sucrase-isomaltase splits sucrose into its component monosaccharides, glucose and fructose. A deficiency of the enzyme leads to sucrose intolerance. We studied the synthesis and intracellular processing of sucrase-isomaltase, using human intestinal explants in organ culture. Pulse-chase experiments with [35S]methionine followed by immunoprecipitation, sodium dodecyl sulfate-polyacrylamide-gel electrophoresis, and fluorography of labeled sucrase-isomaltase demonstrated that the molecule was initially recognized as a protein with a relative molecular weight (Mr) of 205,000. This was apparently converted to a species of 225,000 Mr within two hours. We studied the glycosylation of the protein using endo-beta-N-acetylglucosaminidase H and peptide-N4-(N-acetyl-beta-glucosaminyl)-asparagine amidase digestion of oligosaccharide side chains of the two forms of sucrase-isomaltase. The results showed that the early-appearing 205-kd (kilodalton) molecule contained high-mannose asparagine-linked oligosaccharides, and that the later-appearing, 225-kd molecule contained highly processed (mature) carbohydrate chains. Studies in a patient with primary sucrase-isomaltase deficiency demonstrated normal translation and high-mannose glycosylation of the precursor but a failure in further processing of the oligosaccharides, with subsequent intracellular degradation of the glycoprotein and undetectable enzymatic activity of intestinal sucrase. Abnormal intracellular processing of the enzyme was the probable mechanism of enzyme deficiency in this patient.
Aging is associated with a decline in energy expenditure (EE), glucose intolerance, and a reduction in body nitrogen content. In addition, a reduction in the thermic response to glucose but not to fructose or protein has been reported in the elderly. The present study was conducted to further examine nutrient-induced thermogenesis and the effects of specific sugars on amino acid metabolism in relation to age. After 3 days on a weight-maintaining, 250-g carbohydrate diet, 16 healthy non-obese men and women in two age groups (18 to 29 and 66 to 80 years) consumed on 4 different days 500 mL of either a 75-g fructose or 75-g glucose solution, with or without 300 mg caffeine or vitamin C as a placebo. Blood substrate and hormone levels and EE, using indirect calorimetry, were measured at timed intervals for 3 hours after consumption of the drinks. There was no difference in the carbohydrate-induced increase in EE in either young or old even after adjustments for body weight and fat-free mass (FFM). An approximately 20-fold increase in serum caffeine levels increased EE in both groups (P < .003), but had minimal effects on substrate and hormone responses. In contrast to glucose, fructose induced a marked elevation in plasma alanine from combined basal levels of 301 +/- 24 to approximately 500 +/- 18 mumol/L (mean +/- SEM) in both groups (P < .001). However, both fructose and glucose ingestion resulted in a similar decline in branched-chain and aromatic amino acids.(ABSTRACT TRUNCATED AT 250 WORDS)
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The purpose of the present study was to determine whether fructose is the nutrient mediator of sucrose-induced insulin resistance and glucose intolerance. Toward this end, male rats were fed a purified starch diet (68% of total calories) for a 2-wk baseline period. After this, rats either remained on the starch (ST) diet or were switched to a sucrose (SU, 68% of total calories), fructose/glucose (F/G, 34/34% of total calories), or fructose/starch (F/ST, 34/34% of total calories) diet for 5 wk. Rats then underwent either an intravenous glucose tolerance test (n = 10/diet) or a euglycemic, hyperinsulinemic clamp (n = 8 or 9/diet). Incremental glucose and insulin areas under the curve in SU, F/G, and F/ST were on average 61 and 29% greater than ST, respectively, but not significantly different from one another. During clamps, glucose infusion rates (mg. kg(-1). min(-1)) required to maintain euglycemia were significantly lower (P < 0.05) in SU, F/G, and F/ST (13.4 +/- 0.9, 9. 5 +/- 1.7, 11.3 +/- 1.3, respectively) compared with ST (22.8 +/- 1. 1). Insulin suppression of glucose appearance (mg. kg(-1). min(-1)) was significantly lower (P < 0.05) in SU, F/G, and F/ST (5.6 +/- 0.5, 2.2 +/- 1.2, and 6.6 +/- 0.7, respectively) compared with ST (9.6 +/- 0.4). Insulin-stimulated glucose disappearance (mg. kg(-1). min(-1)) was significantly lower (P < 0.05) in SU, F/G, and F/ST (17. 9 +/- 0.6, 16.2 +/- 1.3, 15.3 +/- 1.8, respectively) compared with ST (24.7 +/- 1.2). These data suggest that fructose is the primary nutrient mediator of sucrose-induced insulin resistance and glucose intolerance.
Deficiency of the membrane protein FAT/CD36 causes a marked defect in fatty acid uptake by various tissues and is genetically linked to insulin resistance in rats and humans. Here, we examined insulin responsiveness of CD36-/- mice. When fed a diet high in complex carbohydrates and low (5%) in fat, these animals cleared glucose faster than the wild-type. In vivo, uptake of 2-fluorodeoxyglucose by muscle was increased severalfold, and in vitro, insulin responsiveness of glycogenesis by the soleus was enhanced. Null mice had lower glycogen levels in muscle and liver, lower muscle triglyceride levels, and increased liver triglyceride content--all findings consistent with increased insulin-sensitivity. However, when the chow diet was switched to one high in fructose, CD36-/- mice but not wild-type mice developed marked glucose intolerance, hyperinsulinemia, and decreased muscle glucose uptake. High-fat diets impaired glucose tolerance equally in both groups, although CD36 deficiency helped moderate insulin-responsive muscle glucose oxidation. In conclusion, CD36 deficiency enhances insulin responsiveness on a high-starch, low-fat diet. It predisposes to insulin resistance induced by high fructose and partially protects from that induced by high-fat diets. In humans, CD36 deficiency may be an important factor in the metabolic adaptation to diet and in susceptibility to some forms of diet-induced pathology.
H (2)- and (13)C-breath tests are valuable non-invasive diagnostic tools for gastroenterological diseases. H (2)-breath tests are clinically established for the diagnosis of carbohydrate intolerance resulting from malabsorption (H (2)-breath tests with lactose, fructose, saccharose, sorbitol), of bacterial overgrowth (glucose H (2)-breath test) and for measurement of orcoceal transit time (lactulose H (2)-breath test). The (13)C-urea breath test is regarded as the "gold standard" procedure for the diagnosis of Helicobacter pylori infection. Moreover, (13)C-breath tests for measurement of gastric emptying can be considered as clinically established, meanwhile. (13)C-breath tests for the evaluation of pancreatic exocrine function or liver function can also be used clinically; however, they currently offer no substantial advantage over other diagnostic procedures. A major disadvantage of all breath tests is that they lack standardization although modifications of the test meal or solution, of the test performance and of the evaluation of data may markedly influence the results. Thus, this article presents the recommendations of the German Society of Neurogastroenterology and Motility and of the German Society of Digestive and Metabolic Diseases for clinically relevant H (2)- and (13)C-breath tests. Indications for the examinations, the procedures to be followed, the analysis of the obtained data and the conclusions to be drawn are delineated. The literature on which the recommendations are based is reviewed. However, personal experience of the authors is also taken into account since numerous questions regarding optimal test performance are not clarified by adequate studies.
Nutritional factors relative to IBS include diagnostic and therapeutic considerations. Etiologically, foods do not cause IBS. A small percentage of patients with childhood allergic diatheses, usually in association with atopic dermatitis and asthma, may be intolerant to one or more of wheat, corn, dairy products, coffee, tea, or citrus fruits. Diagnostically, many patients labeled as IBS subjects are in fact intolerant to the ingestion of lactose-containing foods, sorbitol, fructose, or combinations of fructose and sorbitol. A precise dietary history will characterize this group. Taken in its broadest context, IBS involves the entire hollow tract inclusive of esophagus, stomach, small bowel, and colon. The symptomatic presentation relative to the hollow organ involved allows the selection of dietary manipulations that may help to reduce symptoms. Gastroesophageal reflux, a consequence of low LES pressure in some IBS patients, may be treated with the elimination of fatty foods, alcohol, chocolate, and peppermint. Delayed gastric emptying may be helped by the elimination of fatty foods and reduction of soluble fiber. Aberrant small bowel motor function may be ameliorated by reduction of lactose, sorbitol, and fructose and the addition of soluble fiber. Gas syndromes may be improved by reduced intake of beans, cabbage, lentils, legumes, apples, grapes, and raisins. Colonic motor dysfunction may be overcome by the gradual addition of combinations of soluble and insoluble fiber-containing foods and supplements. The selective use of activated charcoal and simethicone may be helpful.
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