scholarly journals Potassium supplementation, serum immunoreactive insulin concentrations and glucose tolerance in protein-energy malnutrition

1975 ◽  
Vol 33 (1) ◽  
pp. 55-61 ◽  
Author(s):  
M. D. Mann ◽  
Dorothy J. Becker ◽  
B. L. Pimstone ◽  
J. D. L. Hansen
Keyword(s):  
Considerable Increase ◽  
Protein Energy Malnutrition ◽  
Immunoreactive Insulin ◽  
Potassium Depletion ◽  
High Potassium ◽  
Intravenous Glucose ◽  
Potassium Intake ◽  
Serum Immunoreactive Insulin ◽  
Protein Energy ◽  
Impaired Insulin

1. The serum immunoreactive insulin (IRI) concentrations, and glucose disappearance rate-constants after intravenous glucose administration were measured on admission and during recovery in children suffering from protein-energy malnutrition (PEM).2. A high potassium intake resulted in a considerable increase in the serum IRI levels early in the treatment period. There was a definite relationship between potassium depletion and many measurements of insulin secretion.3. The results are consistent with the hypothesis that impaired insulin release in children suffering from PEM is partly the result of potassium depletion.

scholarly journals Glucose Tolerance and Insulin Release in Malnourished Rats

1976 ◽  
Vol 50 (3) ◽  
pp. 153-163 ◽  
Author(s):  
C. Weinkove ◽  
E. A. Weinkove ◽  
B. L. Pimstone
Keyword(s):  
Blood Glucose ◽  
Glucose Tolerance ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Protein Energy Malnutrition ◽  
Insulin Response ◽  
Intravenous Glucose ◽  
Protein Energy

1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a ‘functional immaturity’ of the pancreas.

scholarly journals Circulating ‘big’ insulin in protein-energy malnutrition

1973 ◽  
Vol 30 (2) ◽  
pp. 345-350 ◽  
Author(s):  
Dorothy J. Becker ◽  
Penelope J. Murray ◽  
J. D. L. Hansen ◽  
B. L. Pimstone
Keyword(s):  
Protein Energy Malnutrition ◽  
Significant Negative Correlation ◽  
Insulin Content ◽  
Immunoreactive Insulin ◽  
Total Body Potassium ◽  
Intravenous Injections ◽  
Protein Energy ◽  
Total Body ◽  
Total Iri ◽  
Wide Fluctuation

1. The ‘big’ insulin content of the serums from ten children with protein–energy malnutrition was estimated before, during and after 3–6 weeks of treatment. The values for immunoreactive insulin (IRI) after intravenous injections of glucose were almost normal, with one exception, although tolerance was impaired. In addition, total body potassium content (TBK) was measured for three of the children on each test day.2. In nine of twenty-three estimations ‘big’ insulin content was slightly more than 20% of the total IRI. However, there was a wide fluctuation in the values and no change was noted after treatment.3. The amount of ‘big’ insulin did not correlate with either the magnitude of insulin secretion, the insulin:glucose ratio or TBK. There was a barely significant negative correlation between ‘big’ insulin content and degree of glucose intolerance, with some individual exceptions.

IMPROVEMENT THE PROPERTIES OF YOGHURT USING LEGUMES TO THERAPY PROTEIN ENERGY MALNUTRITION

2018 ◽  
Vol 3 (5) ◽  
pp. 79-88
Author(s):  
Abtsam M.F. Badr ◽  
D.A.M. Amer ◽  
M.Y.A. El- Hawary ◽  
A.M.A. Naem
Keyword(s):  
Protein Energy Malnutrition ◽  
Protein Energy

scholarly journals Sarcopenic Obesity in Liver Cirrhosis: Possible Mechanism and Clinical Impact

2021 ◽  
Vol 22 (4) ◽  
pp. 1917
Author(s):  
Hiroki Nishikawa ◽  
Hirayuki Enomoto ◽  
Shuhei Nishiguchi ◽  
Hiroko Iijima
Keyword(s):  
Liver Cirrhosis ◽  
Current Knowledge ◽  
Protein Energy Malnutrition ◽  
Public Health Problem ◽  
Diagnostic Value ◽  
Sarcopenic Obesity ◽  
Important Public Health Problem ◽  
Alcoholic Fatty Liver ◽  
Protein Energy ◽  
Clinical Consequences

The picture of chronic liver diseases (CLDs) has changed considerably in recent years. One of them is the increase of non-alcoholic fatty liver disease. More and more CLD patients, even those with liver cirrhosis (LC), tend to be presenting with obesity these days. The annual rate of muscle loss increases with worsening liver reserve, and thus LC patients are more likely to complicate with sarcopenia. LC is also characterized by protein-energy malnutrition (PEM). Since the PEM in LC can be invariable, the patients probably present with sarcopenic obesity (Sa-O), which involves both sarcopenia and obesity. Currently, there is no mention of Sa-O in the guidelines; however, the rapidly increasing prevalence and poorer clinical consequences of Sa-O are recognized as an important public health problem, and the diagnostic value of Sa-O is expected to increase in the future. Sa-O involves a complex interplay of physiological mechanisms, including increased inflammatory cytokines, oxidative stress, insulin resistance, hormonal disorders, and decline of physical activity. The pathogenesis of Sa-O in LC is diverse, with a lot of perturbations in the muscle–liver–adipose tissue axis. Here, we overview the current knowledge of Sa-O, especially focusing on LC.

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