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  • Book
    Masaaki Inaba, editor.
    Summary: The aim of this book is to review the latest findings on musculoskeletal disease associated with diabetes. It has been increasingly recognized that maintaining skeletal health is an important factor in achieving longevity in healthy subjects. Diabetes has been established as a disease independently associated with sarcopenia and increased risk of bone fracture resulting from osteoporosis; therefore, it is reasonable to maintain that musculoskeletal health is important in preserving good health. As either bone or muscle is intimately involved in the regulation of metabolic status, keeping the musculoskeletal system healthy is important for improving abnormal glucose metabolism toward normal levels and is vital, as well, for maintaining normal activities of daily living. Muscle is a target of insulin for enhancing the entry of glucose; thus it is conceivable that sarcopenia and muscle containing fat streaks causes insulin resistance in diabetic patients. Furthermore, bone is an organ that regulates Ca and Pi levels in serum by releasing or resorbing Ca and Pi to and from bone tissue. It is now known that bone is a definitive endocrine organ for regulating glucose metabolism and Pi metabolism by secreting osteocalcin and FGF-23 from osteocytes/osteoblasts. Readers will learn of the recent findings in this area, and this book will benefit physicians who deal with diabetes, particularly orthopedists and bone specialists, as well as all physical therapists.

    Contents:
    Part I. Bone Diseases
    1. Bone Disease Associated with Diabetes Mellitus: Particularly Focusing on its Contribution to the Development of Atherosclerosis
    2. Various Kinds of Bone Disease in Diabetes
    Rheumatic Conditions
    3. Fracture Risk in Diabetes
    4. Mechanism for the Development of Bone Disease in Diabetes: Abnormal Glucose Metabolism
    5. Mechanism for the Development of Bone Disease in Diabetes: Increased Oxidative Stress and Advanced Glycation end Products
    6. Mechanism for the Development of Bone Disease in Diabetes: Renal Bone Disease
    7. Impaired Parathyroid Function and Bone Formation-A Risk for Development of Adynamic Bone Disease to Enhance Vascular Calcification
    8. Bone as an Endocrine Organ: Diabetic Bone Disease as a Cause of Endocrine Disorder via Osteocalcin, FGF23 Secreted from Osteocyte/Osteoblast
    Part II. Muscle Diseases
    9. Overview
    10. Mechanism of Skeletal Muscle Contraction: Intracellular Signaling in Skeletal Muscle Contraction
    11. Mechanism of Skeletal Muscle Contraction: Role of Mechanical Muscle Contraction in Glucose Homeostasis
    12. Ectopic Fat Accumulation and Glucose Homeostasis: Ectopic Fat Accumulation in Muscle
    13. Ectopic Fat Accumulation in the Liver and Glucose Homeostasis
    14. Ectopic Fat Accumulation and Glucose Homeostasis: Role of Leptin in Glucose and Lipid Metabolism and Mass Maintenance in Skeletal Muscle
    15. Evaluation of Insulin Resistance in Diabetes: Standard Protocol for a Euglycemic-Hyperinsulinemic Clamp Using an Artificial Pancreas
    16. Sarcopenia in Diabetes Mellitus
    17. Body Temperature Regulation during Exercise Training
    18. Clinical Application of Exercise Therapy in Diabetes
    19. Clinical Application of Exercise Therapy in Diabetes with Chronic Kidney Disease.
    Digital Access Springer 2016
  • Article
    Tamarit-Rodriguez J, Hellman B, Sehilin J.
    Biochim Biophys Acta. 1977 Jan 24;496(1):167-74.
    The effects of the ionophores A-23187 and X-537 A on glucose metabolism, ATP content and sucrose permeability in pancreatic islets microdissected from obese-hyperglycemic mice were studied. The formation of 14CO2 from 10 mM D-[U-14C] GLUCOSE WAS INHIBITED BY OMISSION OF Ca2+ from the medium. A-23187 (10 muM) induced a further decrease of 14CO2 formation whereas X-537 A (10 muM) had no effect. At 20 mM glucose both A-23187 (48 muM) and X-537 A (43 muM) decreased the 14CO2 formation in the absence of Ca2+ whereas only X-537 A inhibited in the presence of Ca2+. X-537 A (43 muM) also decreased the formation of 3H2O from 20 mM D-[5-3H] glucose. The islet content of ATP was not changed after incubation in media deficient in either Mg2+ or Ca2+. However, omission of both Mg2+ and Ca2+ resulted in about 50% decrease of the ATP content. A-23187 and X-537 A induced dose-dependent decreases of the islet ATP content. X-537 A was much more potent than A-23187. Both ionophores induced stronger depression of the ATP content when Ca2+ was omitted. X-537 A (43 muM) but not A-23187 (48 muM) increased the beta-cell membrane permeability as indicated by an increased sucrose space in relation to the urea space of islets. Such an effect was not obtained with X-537 A at 1 muM or by omission of Ca2+. It is suggested that the marked metabolic effects of the ionophores reflect an impaired mitochondrial metabolism. These metabolic changes should be considered in interpretations of ionophore action on insulin secretion.
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