Carbohydrate intolerance in postgastrectomy patients

1966 ◽  
Vol 117 (6) ◽  
pp. 764-768 ◽  
Author(s):  
P. D. Robertson
1985 ◽  
Vol 153 (4) ◽  
pp. 381-385 ◽  
Author(s):  
Larry Cousins ◽  
Bonnie Dattel ◽  
Dorothy Hollingsworth ◽  
Diane Hulbert ◽  
Alfred Zettner

2016 ◽  
Vol 150 (4) ◽  
pp. S43
Author(s):  
Mercedes Amieva-Balmori ◽  
Satish S. Rao ◽  
Enrique Coss-Adame

PEDIATRICS ◽  
1976 ◽  
Vol 57 (2) ◽  
pp. 201-204
Author(s):  
Linda Sue Book ◽  
John J. Herbst ◽  
August L. Jung

A prospective investigation was conducted to determine if infants with necrotizing enterocolitis had evidence of carbohydrate intolerance prior to the onset of clinical symptoms of advanced disease. Stool specimens were examined for fecal reducing substances with Clintest tablets from well, full-term infants and sick premature infants. Only two of 45 (4.4%) formula-fed, full-term infants demonstrated higher than 2 + fecal reducing substances. Ten of 14 (71%) formula-fed premature infants who developed necrotizing enterocolitis had higher than 2 + reducing substances detected in their stools. Daily measurement of fecal reducing substances can be a useful adjunct in the management of sick premature infants.


1991 ◽  
Vol 69 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Clarie B. Hollenbeck ◽  
Ann M. Coulston

A classification of carbohydrate-containing foods based on their glycemic response to 50-g carbohydrate portions has recently been developed. The relative glycemic potency of many of these carbohydrate-containing foods have been compared, and these data have been published in the form of a glycemic index. It has been suggested that meals containing low glycemic index foods will result in a lower postprandial glucose response than meals with a higher glycemic index. However, whether or not these data will lead to a clinically useful reduction in postprandial hyperglycemia in individuals with carbohydrate intolerance remains controversial. In this review, we will try to delineate why we believe that the glycemic index, as currently developed, may be a specious issue. In addition, we will briefly discuss a number of factors that may explain the apparent discrepancy in viewpoints on this issue.Key words: glycemic index, noninsulin-dependent diabetes mellitus, glycemic response, dietary carbohydrate.


1980 ◽  
Vol 96 (6) ◽  
pp. 1009-1014 ◽  
Author(s):  
C. Polychronakos ◽  
J. Letarte ◽  
R. Collu ◽  
J.R. Ducharme

PRILOZI ◽  
2017 ◽  
Vol 38 (3) ◽  
pp. 121-133 ◽  
Author(s):  
Marko Kostovski ◽  
Velibor Tasic ◽  
Nevena Laban ◽  
Momir Polenakovic ◽  
Dragan Danilovski ◽  
...  

AbstractObesity and excess weight are a pandemic phenomenon in the modern world. Childhood and adolescent obesity often ends up in obesity in adults. The costs of obesity and its consequences are staggering for any society, crippling for countries in development. Childhood obesity is also widespread in Macedonia. Metabolic syndrome, dyslipidemia and carbohydrate intolerance are found in significant numbers. Parents and grandparents are often obese. Some of the children are either dysmorphic, or slightly retarded. We have already described patients with Prader-Willi syndrome, Bardet-Biedl syndrome or WAGR syndrome. A genetic screening for mutations in monogenic obesity in children with early, rapid-onset or severe obesity, severe hyperphagia, hypogonadism, intestinal dysfunction, hypopigmentation of hair and skin, postprandial hypoglycaemia, diabetes insipidus, abnormal leptin level and coexistence of lean and obese siblings in the family discovers many genetic forms of obesity. There are about 30 monogenic forms of obesity. In addition, obesity is different in ethnic groups, and the types of monogenic obesity differ. In brief, an increasing number of genes and genetic mechanisms in children continue to be discovered. This sheds new light on the molecular mechanisms of obesity and potentially gives a target for new forms of treatment.


1991 ◽  
Vol 260 (4) ◽  
pp. E513-E520 ◽  
Author(s):  
P. Butler ◽  
E. Kryshak ◽  
R. Rizza

Growth hormone excess can cause postprandial carbohydrate intolerance. To determine the contribution of splanchnic and extrasplanchnic tissues to this process, subjects were fed an isotopically labeled mixed meal after either a 12-h infusion of saline or growth hormone (4 micrograms.kg-1.h-1 [corrected]). Growth hormone infusion resulted in higher glucose and insulin concentrations both before and after meal ingestion. Despite growth hormone-induced hyperglycemia and hyperinsulinemia, postprandial hepatic glucose release and carbon dioxide incorporation into glucose (a qualitative estimate of gluconeogenesis) were similar to those present during saline, suggesting altered hepatic regulation. This was confirmed when glucose was infused in the absence of growth hormone to achieve glucose (and insulin) concentrations comparable to those present during growth hormone infusion. Although growth hormone excess did not alter splanchnic uptake of ingested glucose, it resulted in a fivefold increase in postprandial hepatic glucose release (578 +/- 31 vs. 117 +/- 10 mg.kg-16 h-1, P less than 0.01), less suppression of carbon dioxide incorporation into glucose (-13 +/- 9 vs. -53 +/- 12 mg.kg-1. 6-h-1, P less than 0.01), and lower glucose uptake (1,130 +/- 59 vs. 1,850 +/- 150 mg.kg-1.6 h-1, P less than 0.01). The decrease in postprandial glucose uptake did not appear to be mediated by a change in substrate uptake since postprandial plasma concentrations and forearm balance of lactate, free fatty acids, and ketone bodies did not differ in the presence and absence of growth hormone excess.(ABSTRACT TRUNCATED AT 250 WORDS)


1980 ◽  
Vol 51 (5) ◽  
pp. 1030-1036 ◽  
Author(s):  
JOSEPH PROIETTO ◽  
FRANK P. ALFORD ◽  
FRANK J. DUDLEY

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