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Intro; Preface; Contents; Contributors; Chapter 1: Insulin Resistance in Schizophrenia; 1.1 Introduction; 1.2 Insulin Resistance and Metabolic Syndrome Associated with Antipsychotic Treatment; 1.3 Insulin Resistance in First Onset Antipsychotic Naive Schizophrenia Patients; 1.4 Effects of Insulin Resistance in Schizophrenia on Other Neuroendocrine Systems; 1.4.1 Growth Hormone; 1.4.2 Cortisol; 1.4.3 Gonadal Steroids; 1.4.4 Other Hormones; 1.5 Conclusions; References; Chapter 2: Biogenesis of the Insulin Secretory Granule in Health and Disease; 2.1 Introduction; 2.2 Biosynthesis of Insulin
2.3 Secretion of the Insulin Secretory Granule Contents2.4 Insulin Secretory Granule Contents; 2.4.1 Chromogranin A; 2.4.2 PC1; 2.4.3 PC2; 2.4.4 CPH; 2.4.5 Other Insulin Secretory Granule Proteins; 2.5 Conclusions; References; Chapter 3: Current Models of Fatty Liver Disease; New Insights, Therapeutic Targets and Interventions; 3.1 Introduction; 3.2 NASH Pathogenesis; 3.3 Diet-Induced Models; 3.3.1 High Fat Diet (HFD); 3.3.2 Modified High Fat Diets; 3.3.3 Methionine- and Choline-Deficient Diet (MCD); 3.4 Mechanistic Insights, Susceptibility Factorsand Interventions
3.4.1 Mitochondrial Stress3.4.2 Oxidative Stress; 3.4.3 Inflammation; 3.4.4 Gut-Liver Axis and Microbiome; 3.5 Animal Models to Study Developmental Origins of NAFLD; 3.5.1 Rodents; 3.5.2 Non-human Primates; 3.5.3 Other Models; 3.6 Brain-Liver Axis; 3.7 Conclusions; References; Chapter 4: Preclinical Models of Altered Early Life Nutrition and Development of Reproductive Disorders in Female Offspring; 4.1 Introduction; 4.1.1 Developmental Origins of Health and Disease; 4.1.2 The Importance of Preclinical Models; 4.1.3 Metabolic Effects on Reproductive Health; 4.2 Study Design
4.2.1 Animal Husbandry Guidelines4.2.2 Diets; 4.2.3 Preventing Bias; 4.2.4 Timing; 4.3 Animal Models; 4.3.1 Rodents; 4.3.2 Sheep; 4.3.3 Non-human Primates; 4.4 Models of Reproductive Dysfunction; 4.5 Early-Life Dietary Models and Reproductive Dysfunction; 4.5.1 Undernutrition; 4.5.1.1 Global Undernutrition; 4.5.1.2 Protein Restriction; 4.5.2 Maternal Overnutrition; 4.5.2.1 Single Source High-Fat Diet; 4.5.2.2 Other Single Nutrient Diets; 4.5.2.3 Cafeteria Diet; 4.5.3 Surgical Interventions; 4.6 Conclusions; References
2.3 Secretion of the Insulin Secretory Granule Contents2.4 Insulin Secretory Granule Contents; 2.4.1 Chromogranin A; 2.4.2 PC1; 2.4.3 PC2; 2.4.4 CPH; 2.4.5 Other Insulin Secretory Granule Proteins; 2.5 Conclusions; References; Chapter 3: Current Models of Fatty Liver Disease; New Insights, Therapeutic Targets and Interventions; 3.1 Introduction; 3.2 NASH Pathogenesis; 3.3 Diet-Induced Models; 3.3.1 High Fat Diet (HFD); 3.3.2 Modified High Fat Diets; 3.3.3 Methionine- and Choline-Deficient Diet (MCD); 3.4 Mechanistic Insights, Susceptibility Factorsand Interventions
3.4.1 Mitochondrial Stress3.4.2 Oxidative Stress; 3.4.3 Inflammation; 3.4.4 Gut-Liver Axis and Microbiome; 3.5 Animal Models to Study Developmental Origins of NAFLD; 3.5.1 Rodents; 3.5.2 Non-human Primates; 3.5.3 Other Models; 3.6 Brain-Liver Axis; 3.7 Conclusions; References; Chapter 4: Preclinical Models of Altered Early Life Nutrition and Development of Reproductive Disorders in Female Offspring; 4.1 Introduction; 4.1.1 Developmental Origins of Health and Disease; 4.1.2 The Importance of Preclinical Models; 4.1.3 Metabolic Effects on Reproductive Health; 4.2 Study Design
4.2.1 Animal Husbandry Guidelines4.2.2 Diets; 4.2.3 Preventing Bias; 4.2.4 Timing; 4.3 Animal Models; 4.3.1 Rodents; 4.3.2 Sheep; 4.3.3 Non-human Primates; 4.4 Models of Reproductive Dysfunction; 4.5 Early-Life Dietary Models and Reproductive Dysfunction; 4.5.1 Undernutrition; 4.5.1.1 Global Undernutrition; 4.5.1.2 Protein Restriction; 4.5.2 Maternal Overnutrition; 4.5.2.1 Single Source High-Fat Diet; 4.5.2.2 Other Single Nutrient Diets; 4.5.2.3 Cafeteria Diet; 4.5.3 Surgical Interventions; 4.6 Conclusions; References