Dietary marine fish oils and insulin action in type 2 diabetes

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Supplementation of omega-3 fish oils (n-3 FO) usually worsens the glycemic control in type 2 diabetic subjects. This may be a dose-related phenomenon and is reversed after discontinuation of the n-3 FO supplementation. An increase in the daily caloric intake, due to the fat content of n-3 FO supplements, and a consequent weight gain may contribute to the increase in hyperglycemia. Mechanisms of the increase in hyperglycemia include: (1) n-3 FO may interfere with insulin secretion from the pancreas, and this in turn can cause an increase in the hepatic glucose output and/or a decrease in the glucose uptake by the peripheral tissues; (2) n-3 FO may primarily decrease the sensitivity of liver to insulin action and consequently increase gluconeogenesis and/or glycogenolysis and/or decrease the glycogenesis; (3) n-3 FO may primarily affect the sensitivity of peripheral tissues to insulin, resulting in decreased glucose-uptake; (4) n-3 FO may increase the availability of gluconeogenic substrates by directly altering the partitioning of the metabolic fuels for different pathways in the liver. Direct experimental testing of these possibilities has been difficult, because n-3 FO affects the carbohydrate metabolism differently in animal models than in humans. The available data suggest that n-3 FO inhibits insulin secretion in response to glucose load, mixed meal, and glucagon but not at the fasting state. Hepatic glucose output is increased. Sensitivity of the peripheral tissues to insulin is not changed. An encouraging observation is that the hyperglycemic effect of n-3 FO may decrease with time even when therapy is continued. Proper use of this treatment modality requires careful evaluation of the risk/benefit ratio for every individual patient.

Original languageEnglish (US)
Pages (from-to)250-257
Number of pages8
JournalAnnals of the New York Academy of Sciences
Volume683
StatePublished - 1993

Fingerprint

Fish Oils
Medical problems
Type 2 Diabetes Mellitus
Insulin
Glucose
Liver
Tissue
Hyperglycemia
Glycogenolysis
Gluconeogenesis
Carbohydrate Metabolism
Energy Intake
Glucagon
Weight Gain
Meals
Pancreas
Fasting
Animals
Animal Models
Fats

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Dietary marine fish oils and insulin action in type 2 diabetes. / Karakas, Siddika E.

In: Annals of the New York Academy of Sciences, Vol. 683, 1993, p. 250-257.

Research output: Contribution to journalArticle

@article{5bdb254419e44054872c7f05524bd0c8,
title = "Dietary marine fish oils and insulin action in type 2 diabetes",
abstract = "Supplementation of omega-3 fish oils (n-3 FO) usually worsens the glycemic control in type 2 diabetic subjects. This may be a dose-related phenomenon and is reversed after discontinuation of the n-3 FO supplementation. An increase in the daily caloric intake, due to the fat content of n-3 FO supplements, and a consequent weight gain may contribute to the increase in hyperglycemia. Mechanisms of the increase in hyperglycemia include: (1) n-3 FO may interfere with insulin secretion from the pancreas, and this in turn can cause an increase in the hepatic glucose output and/or a decrease in the glucose uptake by the peripheral tissues; (2) n-3 FO may primarily decrease the sensitivity of liver to insulin action and consequently increase gluconeogenesis and/or glycogenolysis and/or decrease the glycogenesis; (3) n-3 FO may primarily affect the sensitivity of peripheral tissues to insulin, resulting in decreased glucose-uptake; (4) n-3 FO may increase the availability of gluconeogenic substrates by directly altering the partitioning of the metabolic fuels for different pathways in the liver. Direct experimental testing of these possibilities has been difficult, because n-3 FO affects the carbohydrate metabolism differently in animal models than in humans. The available data suggest that n-3 FO inhibits insulin secretion in response to glucose load, mixed meal, and glucagon but not at the fasting state. Hepatic glucose output is increased. Sensitivity of the peripheral tissues to insulin is not changed. An encouraging observation is that the hyperglycemic effect of n-3 FO may decrease with time even when therapy is continued. Proper use of this treatment modality requires careful evaluation of the risk/benefit ratio for every individual patient.",
author = "Karakas, {Siddika E}",
year = "1993",
language = "English (US)",
volume = "683",
pages = "250--257",
journal = "Annals of the New York Academy of Sciences",
issn = "0077-8923",
publisher = "Wiley-Blackwell",

}

TY - JOUR

T1 - Dietary marine fish oils and insulin action in type 2 diabetes

AU - Karakas, Siddika E

PY - 1993

Y1 - 1993

N2 - Supplementation of omega-3 fish oils (n-3 FO) usually worsens the glycemic control in type 2 diabetic subjects. This may be a dose-related phenomenon and is reversed after discontinuation of the n-3 FO supplementation. An increase in the daily caloric intake, due to the fat content of n-3 FO supplements, and a consequent weight gain may contribute to the increase in hyperglycemia. Mechanisms of the increase in hyperglycemia include: (1) n-3 FO may interfere with insulin secretion from the pancreas, and this in turn can cause an increase in the hepatic glucose output and/or a decrease in the glucose uptake by the peripheral tissues; (2) n-3 FO may primarily decrease the sensitivity of liver to insulin action and consequently increase gluconeogenesis and/or glycogenolysis and/or decrease the glycogenesis; (3) n-3 FO may primarily affect the sensitivity of peripheral tissues to insulin, resulting in decreased glucose-uptake; (4) n-3 FO may increase the availability of gluconeogenic substrates by directly altering the partitioning of the metabolic fuels for different pathways in the liver. Direct experimental testing of these possibilities has been difficult, because n-3 FO affects the carbohydrate metabolism differently in animal models than in humans. The available data suggest that n-3 FO inhibits insulin secretion in response to glucose load, mixed meal, and glucagon but not at the fasting state. Hepatic glucose output is increased. Sensitivity of the peripheral tissues to insulin is not changed. An encouraging observation is that the hyperglycemic effect of n-3 FO may decrease with time even when therapy is continued. Proper use of this treatment modality requires careful evaluation of the risk/benefit ratio for every individual patient.

AB - Supplementation of omega-3 fish oils (n-3 FO) usually worsens the glycemic control in type 2 diabetic subjects. This may be a dose-related phenomenon and is reversed after discontinuation of the n-3 FO supplementation. An increase in the daily caloric intake, due to the fat content of n-3 FO supplements, and a consequent weight gain may contribute to the increase in hyperglycemia. Mechanisms of the increase in hyperglycemia include: (1) n-3 FO may interfere with insulin secretion from the pancreas, and this in turn can cause an increase in the hepatic glucose output and/or a decrease in the glucose uptake by the peripheral tissues; (2) n-3 FO may primarily decrease the sensitivity of liver to insulin action and consequently increase gluconeogenesis and/or glycogenolysis and/or decrease the glycogenesis; (3) n-3 FO may primarily affect the sensitivity of peripheral tissues to insulin, resulting in decreased glucose-uptake; (4) n-3 FO may increase the availability of gluconeogenic substrates by directly altering the partitioning of the metabolic fuels for different pathways in the liver. Direct experimental testing of these possibilities has been difficult, because n-3 FO affects the carbohydrate metabolism differently in animal models than in humans. The available data suggest that n-3 FO inhibits insulin secretion in response to glucose load, mixed meal, and glucagon but not at the fasting state. Hepatic glucose output is increased. Sensitivity of the peripheral tissues to insulin is not changed. An encouraging observation is that the hyperglycemic effect of n-3 FO may decrease with time even when therapy is continued. Proper use of this treatment modality requires careful evaluation of the risk/benefit ratio for every individual patient.

UR - http://www.scopus.com/inward/record.url?scp=0027301891&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027301891&partnerID=8YFLogxK

M3 - Article

C2 - 8352447

AN - SCOPUS:0027301891

VL - 683

SP - 250

EP - 257

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

ER -