Table Of ContentENDOCRINOLOGY RESEARCH AND CLINICAL DEVELOPMENTS
I R
NSULIN ESISTANCE
N D
EW EVELOPMENTS
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E R
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ENDOCRINOLOGY RESEARCH AND CLINICAL DEVELOPMENTS
I R
NSULIN ESISTANCE
N D
EW EVELOPMENTS
JOHN FREEMAN
AND
SCOTT NEWMAN
EDITORS
New York
Copyright © 2013 by Nova Science Publishers, Inc.
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CONTENTS
Preface vii
Chapter 1 Pathophysiological Basis for Antioxidant Therapy
of Insulin Resistance 1
Ramón Rodrigo, Matías Libuy
and Jaime González
Chapter 2 New Insight into the Regulation of Insulin
Resistance 41
Penghua Fang, Mingyi Shi, Mei Yu
and Ping Bo
Chapter 3 Insulin Resistance after Severe Burn Injury 67
Hongzhi Xu and Yong-Ming Yu
Chapter 4 Lipoprotein Lipase and Insulin Resistance 87
Masataka Kusunoki
Index 103
PREFACE
The hallmark of insulin resistance is an obstacle to glucose uptake,
resulting in hyperglycemia and hyperinsulinemia as well as type 2 diabetes
mellitus. The prevalence of diabetes mellitus is rapidly increasing worldwide
and is becoming an important health problem. In this book, the authors present
current research in the study of insulin resistance including: the
pathophysiological basis for antioxidant therapy of insulin resistance; new
insight into the regulation of insulin resistance; burn injury and its association
with insulin resistance and hyperglycemia which complicates clinical
management; and lipoprotein lipase and its role in insulin resistance.
Chapter 1 – The biochemical steps linking insulin resistance with the
metabolic syndrome have not been completely clarified. Mounted
experimental and clinical evidence indicates that oxidative stress is an
attractive candidate for a central pathogenic role since it potentially explains
the appearance of all risk factors and supports the clinical manifestations.
Indeed, metabolic syndrome patients exhibit activation of biochemical
pathways leading to increased delivery of ROS, decreased antioxidant
protection and increased lipid peroxidation. The described associations
between increased abdominal fat storage, liver steatosis and systemic oxidative
stress, the diminished concentration of nitric oxide derivatives and antioxidant
vitamins, and the endothelial oxidative damages observed in subjects with the
metabolic syndrome support oxidative stress as the common second-level
event in an unifying pathogenic view. Moreover, it has been observed that
oxidative stress regulates the expression of genes governing lipid and glucose
metabolism through activation or inhibition of intracellular sensors. Diet
constituents can modulate redox reactions and the oxidative stress extent, thus
also acting on nuclear gene expression. As a consequence of the food–gene
viii John Freeman and Scott Newman
interaction, metabolic syndrome patients may express different disease
features and extents according to the different pathways activated by oxidative
stress-modulated effectors. This view could also explain family differences
and interethnic variations in determining risk factor appearance.
Chapter 2 – Insulin resistance is characterized by decreased glucose
uptake and tissue sensitivity to insulin stimulation despite normal or elevated
insulin concentration. There is an upward trend in the incidence of insulin
resistance in developed countries. Despite considerable research into the
etiology, the precise mechanism underlying the disorder still remains elusive.
Both genetic and postnatal factors, especially increased diet caloricity and
decreased physical activity, play an important role in the etiology of insulin
resistance. Recent studies have provided compelling clues about insulin
resistance. This review examines the updated information for insulin
resistance, highlighting the effect of endocrine hormones on insulin resistance
and glucose homeostasis, including galanin, ghrelin, leptin, adiponectin and
retinol-binding protein 4. In addition, this paper introduces the roles of the
autonomic nervous system, intestinal microbiota, peroxisome proliferator-
activated receptors and Vitamin D deficiency in regulating insulin resistance.
Furthermore, the article presents current guidelines for risk factors for
developing insulin resistance, direct and indirect assessment methods of
insulin resistance, as well as the new insight into primary prevention and
therapy of insulin resistance. It may foresee that this research line will bring a
new ideal in diagnostics and alleviation of insulin resistance.
Chapter 3 – Objective. Burn injury (BI) is associated with insulin
resistance and hyperglycemia which complicate clinical management. The
authors investigated the impact of BI on glucose metabolism in a rabbit model
of burn injury using a combination of PET and stable isotope studies under
euglycemic insulin clamp (EIC) conditions.
Materials/Methods. Twelve male rabbits were subjected to either full
thickness burn injury (B) or sham burn (SB). Three days after treatment, an
EIC condition was established by constant infusion of insulin, concomitantly
with a variable rate of dextrose infusion. PET imaging of the hind limbs was
conducted to determine the rates of peripheral O2 and glucose utilization. Each
animal also received a primed constant infusion of [6,6,2H2] glucose to
determine endogenous glucose production.
Results. The fasting blood glucose in the burned rabbits was higher than in
the sham group. Under EIC conditions, the SB group required more exogenous
dextrose than the B group in order to maintain blood glucose at physiological
levels (22.2 ± 2.6 vs 13.3 ± 2.9 mg/min, P < 0.05), indicating a state of insulin
