scholarly journals Suppression of Free Fatty Acids by Oral Glucose in Patients with Cystic Fibrosis

2019 ◽  
Vol 3 (1) ◽  
Author(s):  
Schnyder Marie-Angela ◽  
Tschopp Oliver ◽  
Zwimpfer Cornelia ◽  
Benden Christian ◽  
Schmid Christoph
Keyword(s):  
Cystic Fibrosis ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Oral Glucose

Metabolic Research in Monozygotic Twins with Diabetes Mellitus: Progress Report

1976 ◽  
Vol 25 (1) ◽  
pp. 281-288
Author(s):  
T. Goecke ◽  
W. Grote ◽  
D. Grueneklee
Keyword(s):  
Diabetes Mellitus ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Monozygotic Twins ◽  
Characteristic Parameter ◽  
Tolerance Test ◽  
Immunoreactive Insulin ◽  
Oral Glucose ◽  
Juvenile Diabetics ◽  
Intravenous Tolbutamide Test

An intravenous and oral glucose tolerance test and an intravenous tolbutamide test have been performed in 11 MZ twin pairs, discordant for diabetes mellitus. Blood sugar, immunoreactive insulin, and free fatty acids were determined. The research aimed at finding out whether prediabetic subjects may show any characteristic parameter which could be suggestive of the hereditary disposition. Three MZ twins of juvenile diabetics showed a normal blood glucose, immunoreactive insulin, and free fatty acids during the glucose and tolbutamide loads within a maximum of 10 years observation.

THE ROLE OF PLASMA FREE FATTY ACIDS IN THE ELEVATION OF PLASMA CHOLESTEROL AND PHOSPHOLIPIDS PRODUCED BY ADRENALINE

1966 ◽  
Vol 36 (3) ◽  
pp. 301-316 ◽  
Author(s):  
A. M. BARRETT
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Plasma Cholesterol ◽  
Hormone Secretion ◽  
Oral Glucose ◽  
Plasma Free Fatty Acids ◽  
Plasma Ffa ◽  
Adrenocortical Hormone ◽  
Glucose Plasma ◽  
Acute Changes

SUMMARY The effects of adrenaline, noradrenaline, corticotrophin (ACTH), cortisol and corticosterone on the levels of blood lipids have been studied in dogs and rats. Blood glucose, plasma free fatty acids (FFA) and corticosteroids were determined 4 hr. after injection. Plasma cholesterol, phospholipids and triglycerides were determined 24 hr. after the last of three daily treatments. In some experiments an oral glucose load was given at the same time as the hormones. In dogs plasma FFA were increased by adrenaline and noradrenaline, decreased by ACTH plus glucose and not affected by ACTH alone. Gradual rises in the lipoprotein levels of dogs were produced by any of the hormones given and followed acute rises in corticosteroid concentration regardless of the acute changes in plasma FFA. In rats plasma FFA were increased by adrenaline and ACTH, decreased by glucose and not affected by ACTH plus glucose. It was not possible to produce rises in lipoprotein by administering adrenaline or ACTH to rats. Exogenous corticosteroids produced increases in the cholesterol and phospholipid levels. The effects of corticosterone were potentiated by oral glucose but cortisol produced a full effect without extra glucose. The FFA responses to subcutaneous adrenaline in rats were reduced by adrenalectomy, but the increases in plasma FFA produced by intravenous infusion of adrenaline or ACTH were similar in adrenalectomized and intact rats. It was concluded that changes in lipoproteins are not causally related to increased mobilization of FFA but are dependent on increased adrenocortical hormone secretion in the presence of excess carbohydrate.

scholarly journals Free fatty acids, glicentin and glucose-dependent insulinotropic polypeptide as potential major determinants of fasting substrate oxidation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Julia Hummel ◽  
Louise Fritsche ◽  
Andreas Vosseler ◽  
Corinna Dannecker ◽  
Miriam Hoene ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Free Fatty Acids ◽  
Body Fat ◽  
Respiratory Quotient ◽  
Substrate Oxidation ◽  
Oral Glucose ◽  
Fasting State ◽  
The Metabolic Syndrome ◽  
Fuel Selection

AbstractThe selection of carbohydrates or fat to generate intracellular energy is thought to be crucial for long-term metabolic health. While most studies assess fuel selection after a metabolic challenge, the determinants of substrate oxidation in the fasted state remain largely unexplored. We therefore assessed the respiratory quotient by indirect calorimetry as a read-out for substrate oxidation following an overnight fast. This cross-sectional analysis consisted of 192 (92 women, 100 men) either lean or obese participants. Following an overnight fast, the respiratory quotient (RQ) was assessed, after which a 5-point 75-g oral glucose tolerance test was performed. Unlike glucose and insulin, fasting free fatty acids (FFA) correlated negatively with fasting RQ (p < 0.0001). Participants with high levels of the ketone body β-hydroxybutyric acid had significantly lower RQ values. Fasting levels of glucose-dependent insulinotropic polypeptide (GIP) and glicentin were positively associated with fasting RQ (all p ≤ 0.03), whereas GLP-1 showed no significant association. Neither BMI, nor total body fat, nor body fat distribution correlated with fasting RQ. No relationship between the RQ and diabetes or the metabolic syndrome could be observed. In the fasting state, FFA concentrations were strongly linked to the preferentially oxidized substrate. Our data did not indicate any relationship between fasting substrate oxidation and metabolic diseases, including obesity, diabetes, and the metabolic syndrome. Since glicentin and GIP are linked to fuel selection in the fasting state, novel therapeutic approaches that target these hormones may have the potential to modulate substrate oxidation.

Evidence for an Hepatic Anti-Ketogenic Effect of Insulin in Man

1978 ◽  
Vol 55 (5) ◽  
pp. 499-504 ◽  
Author(s):  
R. S. Elkeles ◽  
R. A. Chalmers ◽  
J. Hambley
Keyword(s):  
Fatty Acids ◽  
Insulin Secretion ◽  
Free Fatty Acids ◽  
Direct Effect ◽  
Normal Subjects ◽  
Oral Glucose ◽  
Plasma Free Fatty Acids ◽  
Sharp Fall ◽  
Plasma Ffa ◽  
Effect Of Glucose

1. Infusion of a triglyceride emulsion (Intralipid) into overnight fasted normal subjects produced a rise in plasma free fatty acids (FFA) and blood ketones. 2. Glucose given orally 60 min after the start of the Intralipid infusion produced a sharp fall in blood ketones without much change in plasma FFA. 3. An infusion of glucagon given together with Intralipid did not alter the reduction in blood ketones produced by oral glucose in normal subjects. 4. Oral glucose given 60 min after the start of the Intralipid infusion in three insulin-requiring diabetic subjects produced no fall in blood ketones. 5. The results suggest that glucose prevents the increase in blood ketones after Intralipid through an increase in insulin secretion rather than through a suppression of glucagon or as a direct effect of glucose. 6. It is most likely that the effect of insulin is to inhibit hepatic ketogenesis.

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