Alcohol Use Behaviors, Fat Intake and the Function of Pancreatic β-Cells in Non-Obese, Healthy Korean Males: Findings from 2010 Korea National Health and Nutrition Examination Survey

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Aims: In the present study, we aimed to identify dietary factors related to insulin secretion function especially in healthy, non-obese Korean males. Methods: Data were obtained from the Korea National Health and Nutrition Examination Survey V-1 (KNHANES V-1). Nine hundred and twenty male adults aged >30 years of normal weight were included, excluding those with type 2 diabetes mellitus and liver disease. Alcohol use disorders identification test (AUDIT) score which represents alcohol use behaviors and nutrient intakes was used, and homeostasis model assessment of β-cell function (HOMA-B score) was calculated. Results: HOMA-B scorewas associated with age (p < 0.001), AUDIT score (p = 0.030), and percentage of fat from total energy intake (p = 0.002). HOMA-B scores in the problematic AUDIT group were significantly lower than those in the normal AUDIT group. In addition, HOMA-B scores in the lowest fat intake group were significantly lower than those in the medium fat intake group, but similar to those in the highest fat intake group. There was an interaction between alcohol use behaviors and percentage of fat from energy intake in determining HOMA-B score (p for interaction = 0.034). Conclusions: Alcohol use behaviors and percentage of fat from energy intake were found to be associated with HOMA-B score in healthy, non-obese Korean males.

Related collections

Most cited references 26

Record: found
Abstract: found
Article: found

Is Open Access

Full Accounting of Diabetes and Pre-Diabetes in the U.S. Population in 1988–1994 and 2005–2006

Catherine C Cowie, Keith F. Rust, Earl S. Ford … (2009)

OBJECTIVE—We examined the prevalences of diagnosed diabetes, and undiagnosed diabetes and pre-diabetes using fasting and 2-h oral glucose tolerance test values, in the U.S. during 2005–2006. We then compared the prevalences of these conditions with those in 1988–1994. RESEARCH DESIGN AND METHODS—In 2005–2006, the National Health and Nutrition Examination Survey included a probability sample of 7,267 people aged ≥12 years. Participants were classified according to glycemic status by interview for diagnosed diabetes and by fasting and 2-h glucoses measured in subsamples. RESULTS—In 2005–2006, the crude prevalence of total diabetes in people aged ≥20 years was 12.9%, of which ∼40% was undiagnosed. In people aged ≥20 years, the crude prevalence of impaired fasting glucose was 25.7% and of impaired glucose tolerance was 13.8%, with almost 30% having either. Over 40% of individuals had diabetes or pre-diabetes. Almost one-third of the elderly had diabetes, and three-quarters had diabetes or pre-diabetes. Compared with non-Hispanic whites, age- and sex-standardized prevalence of diagnosed diabetes was approximately twice as high in non-Hispanic blacks (P < 0.0001) and Mexican Americans (P = 0.0001), whereas undiagnosed diabetes was not higher. Crude prevalence of diagnosed diabetes in people aged ≥20 years rose from 5.1% in 1988–1994 to 7.7% in 2005–2006 (P = 0.0001); this was significant after accounting for differences in age and sex, particularly in non-Hispanic blacks. Prevalences of undiagnosed diabetes and pre-diabetes were generally stable, although the proportion of total diabetes that was undiagnosed decreased in Mexican Americans. CONCLUSIONS—Over 40% of people aged ≥20 years have hyperglycemic conditions, and prevalence is higher in minorities. Diagnosed diabetes has increased over time, but other conditions have been relatively stable.

0 comments Cited 266 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Pathogenesis of NIDDM. A balanced overview.

R DeFronzo, R C Bonadonna, E Ferrannini (1992)

Non-insulin-dependent diabetes mellitus (NIDDM) results from an imbalance between insulin sensitivity and insulin secretion. Both longitudinal and cross-sectional studies have demonstrated that the earliest detectable abnormality in NIDDM is an impairment in the body's ability to respond to insulin. Because the pancreas is able to appropriately augment its secretion of insulin to offset the insulin resistance, glucose tolerance remains normal. With time, however, the beta-cell fails to maintain its high rate of insulin secretion and the relative insulinopenia (i.e., relative to the degree of insulin resistance) leads to the development of impaired glucose tolerance and eventually overt diabetes mellitus. The cause of pancreatic "exhaustion" remains unknown but may be related to the effect of glucose toxicity in a genetically predisposed beta-cell. Information concerning the loss of first-phase insulin secretion, altered pulsatility of insulin release, and enhanced proinsulin-insulin secretory ratio is discussed as it pertains to altered beta-cell function in NIDDM. Insulin resistance in NIDDM involves both hepatic and peripheral, muscle, tissues. In the postabsorptive state hepatic glucose output is normal or increased, despite the presence of fasting hyperinsulinemia, whereas the efficiency of tissue glucose uptake is reduced. In response to both endogenously secreted or exogenously administered insulin, hepatic glucose production fails to suppress normally and muscle glucose uptake is diminished. The accelerated rate of hepatic glucose output is due entirely to augmented gluconeogenesis. In muscle many cellular defects in insulin action have been described including impaired insulin-receptor tyrosine kinase activity, diminished glucose transport, and reduced glycogen synthase and pyruvate dehydrogenase. The abnormalities account for disturbances in the two major intracellular pathways of glucose disposal, glycogen synthesis, and glucose oxidation. In the earliest stages of NIDDM, the major defect involves the inability of insulin to promote glucose uptake and storage as glycogen. Other potential mechanisms that have been put forward to explain the insulin resistance, include increased lipid oxidation, altered skeletal muscle capillary density/fiber type/blood flow, impaired insulin transport across the vascular endothelium, increased amylin, calcitonin gene-related peptide levels, and glucose toxicity.

0 comments Cited 217 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Long-term exposure of rat pancreatic islets to fatty acids inhibits glucose-induced insulin secretion and biosynthesis through a glucose fatty acid cycle.

V. Grill, Ying Zhou (1994)

We tested effects of long-term exposure of pancreatic islets to free fatty acids (FFA) in vitro on B cell function. Islets isolated from male Sprague-Dawley rats were exposed to palmitate (0.125 or 0.25 mM), oleate (0.125 mM), or octanoate (2.0 mM) during culture. Insulin responses were subsequently tested in the absence of FFA. After a 48-h exposure to FFA, insulin secretion during basal glucose (3.3 mM) was several-fold increased. However, during stimulation with 27 mM glucose, secretion was inhibited by 30-50% and proinsulin biosynthesis by 30-40%. Total protein synthesis was similarly affected. Conversely, previous palmitate did not impair alpha-ketoisocaproic acid (5 mM)-induced insulin release. Induction and reversibility of the inhibitory effect on glucose-induced insulin secretion required between 6 and 24 h. Addition of the carnitine palmitoyltransferase I inhibitor etomoxir (1 microM) partially reversed (by > 50%) FFA-associated decrease in secretory as well as proinsulin biosynthetic responses to 27 mM glucose. The inhibitory effect of previous palmitate was similar when co-culture was performed with 5.5, 11, or 27 mM glucose. Exposure to palmitate or oleate reduced the production of 14CO2 from D-[U-14C]glucose, and of 14CO2 from D-[3,4-14C]-glucose, both effects being reversed by etomoxir. long-term exposure to FFA inhibits glucose-induced insulin secretion and biosynthesis probably through a glucose fatty acid cycle.

0 comments Cited 94 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (publisher-id): ANM

Journal ID (nlm-ta): Ann Nutr Metab

Journal ID (doi): 10.1159/issn.0250-6807

Title: Annals of Nutrition and Metabolism

Publisher: S. Karger AG

ISSN (Print): 0250-6807

ISSN (Electronic): 1421-9697

Publication date Subscription-year: 2013

Publication date (Print): March 2013

Publication date (Electronic): 31 January 2013

Volume: 62

Issue: 2

Pages: 129-136

Affiliations

^aDepartment of Food and Nutrition, Korea University, ^bDepartment of Nutrition Services, Gangnam Severance Hospital, Yonsei University, Seoul, South Korea

Author notes

*Assoc. Prof. Min-Jeong Shin, Department of Food and Nutrition, Korea University, Seoul 136-703 (South Korea), E-Mail mjshin@korea.ac.kr

Article

Publisher ID: 345587 Other ID: Ann Nutr Metab 2013;62:129–136

DOI: 10.1159/000345587

PubMed ID: 23392227

SO-VID: ff7902e8-d3e3-4381-bf0d-ff1d9f5ed62b

License:

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 10 August 2012

Date accepted : 27 October 2012

Page count

Figures: 1, Tables: 4, Pages: 8

Comments

Comment on this article

scite_

Cited by 2

See all cited by

Most referenced authors 523

See all reference authors

- Version 1

Alcohol Use Behaviors, Fat Intake and the Function of Pancreatic β-Cells in Non-Obese, Healthy Korean Males: Findings from 2010 Korea National Health and Nutrition Examination Survey

Read this article at

Abstract

Related collections

Karger: Nutrition and Dietetics

Most cited references 26

Full Accounting of Diabetes and Pre-Diabetes in the U.S. Population in 1988–1994 and 2005–2006

Pathogenesis of NIDDM. A balanced overview.

Long-term exposure of rat pancreatic islets to fatty acids inhibits glucose-induced insulin secretion and biosynthesis through a glucose fatty acid cycle.

Author and article information

Journal

Affiliations

Author notes

Article

History

Page count

Categories

Comments

Comment on this article

Similar content 117

Cited by 2

Most referenced authors 523