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Insulin And Bone Growth

Diabetes And Bone Mass

Diabetes And Bone Mass

What is the link between diabetes (both type 1 and type 2) and bone mineral density/osteoporosis? Response from Stephen Schneider, MD It has been more than 50 years since Drs. Albright and Reifenstein demonstrated that diabetes could be associated with loss of bone mass. Since that time, the relationship between osteopenia and type 1 diabetes has become well established, while the effects of type 2 diabetes on bone metabolism have remained less clear. One recent study[ 1 ] demonstrated a greater than 12-fold higher risk for hip fractures in women with type 1 diabetes compared with the general population. Women with type 2 diabetes had a still significant but much smaller 1.7-fold increase in risk. Patients with type 2 diabetes taking insulin had a greater risk than patients taking oral agents or than patients not on pharmacotherapy, suggesting that the severity of the metabolic abnormalities might be related to the subsequent risk of fracture. Interpretation of fracture data as a surrogate measure for bone metabolism is particularly difficult in patients with long-standing diabetes,[ 2 ] because visual and neurologic complications can predispose patients to accidents resulting in an increased fracture risk not necessarily dependent on bone density alone. Other factors that make studies difficult to interpret include the presence of diabetic renal disease, autonomic and other neuropathic changes that could contribute to a loss of bone mineral,[ 3 ] and a low level of physical activity related to diabetic complications. Also, women with diabetes are much less likely to be on estrogen replacement therapy. What metabolic factors could contribute to the apparent abnormalities of bone metabolism in diabetes? In animal models of insulin-deficient diabetes, both decreased bone Continue reading >>

Anabolic Effects Of Insulin On Bone Suggest A Role For Chromium Picolinate In Preservation Of Bone Density

Anabolic Effects Of Insulin On Bone Suggest A Role For Chromium Picolinate In Preservation Of Bone Density

Volume 45, Issue 3 , September 1995, Pages 241-246 Anabolic effects of insulin on bone suggest a role for chromium picolinate in preservation of bone density Author links open overlay panel M.F.McCarty Get rights and content Activation of osteoclasts by parathyroid hormone (PTH) is mediated by PTH stimulation of osteoblasts, and is dependent on a PTH-induced rise in protein kinase C activity. Physiological levels of insulin reduce the ability of PTH to activate protein kinase C in osteoblasts, suggesting that insulin may be a physiological antagonist of bone resorption. In addition, insulin is known to promote collagen production by osteoblasts. These findings imply that efficient insulin activity may exert an anabolic effect on bone, and rationalize the many clinical studies demonstrating reduced bone density in Type I diabetes. Recently, the insulin-sensitizing nutrient chromium picolinate has been found to reduce urinary excretion of hydroxyproline and calcium in postmenopausal women, presumably indicative of a reduced rate of bone resorption. This nutrient also raised serum levels of dehydroepiandrosterone-sulfate, which may play a physiological role in the preservation of postmenopausal bone density. The impact of chromium picolinate (alone or in conjunction with calcium and other micronutrients) on bone metabolism and bone density, merits further evaluation in controlled studies. Continue reading >>

Normal Bone Density Obtained In The Absence Of Insulin Receptor Expression In Bone

Normal Bone Density Obtained In The Absence Of Insulin Receptor Expression In Bone

Type I diabetes is characterized by little or no insulin production and hyperglycemic conditions. It is also associated with significant bone loss and increased bone marrow adiposity. To examine the role of reduced insulin signaling in type I diabetic bone loss without inducing hyperglycemia, we used genetically reconstituted insulin receptor knockout mice (IRKO-L1) that are euglycemic as a result of human insulin receptor transgene expression in the pancreas, liver, and brain. RT-PCR analyses demonstrated undetectable levels of insulin receptor expression in IRKO-L1 bone, yet IRKO-L1 bones exhibit similar (and trend toward greater) bone density compared with wild-type animals as determined by microcomputed tomography. More detailed bone analyses indicated that cortical bone area was increased in tibias of IRKO-L1 mice. Osteoblast markers (osteocalcin and runx2 mRNA levels) and resorption markers (serum pyridinoline levels) were similar in wild-type and IRKO-L1 bones. When marrow adiposity was examined, we noticed a decrease in adipocyte number and fatty-acid-binding protein 2 expression in IRKO-L1 mice compared with wild-type mice. Bone marrow stromal cell cultures obtained from wild-type and IRKO-L1 mice demonstrated similar adipogenic and osteogenic potentials, indicating that systemic factors likely contribute to differences in marrow adiposity in vivo. Interestingly, IGF-I receptor mRNA levels were elevated in IRKO-L1 bones, suggesting (in combination with hyperinsulinemic conditions) that increased IGF-I receptor signaling may represent a compensatory response and contribute to the changes in cortical bone. Taken together, these results suggest that reduced insulin receptor signaling in bone is not a major factor contributing to bone loss in type I diabetes. INSU Continue reading >>

Jci -insulin, Osteoblasts, And Energy Metabolism: Why Bone Counts Calories

Jci -insulin, Osteoblasts, And Energy Metabolism: Why Bone Counts Calories

Insulin, osteoblasts, and energy metabolism: why bone counts calories Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Baltimore Veterans Administration Medical Center, Baltimore, Maryland, USA. Address correspondence to: Thomas L. Clemens, Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, 601 N. Caroline St., Baltimore, Maryland 21287, USA. Phone: 410.955.3245; Fax: 410.614.1451; E-mail: [email protected] . Find articles by Riddle, R. in: JCI | PubMed | Google Scholar Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Baltimore Veterans Administration Medical Center, Baltimore, Maryland, USA. Address correspondence to: Thomas L. Clemens, Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, 601 N. Caroline St., Baltimore, Maryland 21287, USA. Phone: 410.955.3245; Fax: 410.614.1451; E-mail: [email protected] . Find articles by Clemens, T. in: JCI | PubMed | Google Scholar First published March 18, 2014- More info Published in Volume 124, Issue 4 (April 1, 2014) J Clin Invest.2014;124(4):14651467. . Copyright 2014, The American Society for Clinical Investigation. Insulin signaling in osteoblasts has been shown recently to contribute to whole-body glucose homeostasis in animals fed a normal diet; however, it is unknown whether bone contributes to the insulin resistance that develops in animals challenged by a high-fat diet (HFD). Here, we evaluated the consequences of osteoblast-specific overexpression of or loss of insulin receptor in HFD-fed mice. We determined that the severity of glucose intolerance and insulin resistance that mice develop when fed a HFD is in part a consequence of osteoblast-dependent Continue reading >>

Impact Of Diabetes And Diabetes Medications On Bone Health | Endocrine Reviews | Oxford Academic

Impact Of Diabetes And Diabetes Medications On Bone Health | Endocrine Reviews | Oxford Academic

Patients with type 2 diabetes mellitus (T2DM) have an increased risk of fragility fractures despite increased body weight and normal or higher bone mineral density. The mechanisms by which T2DM increases skeletal fragility are unclear. It is likely that a combination of factors, including a greater risk of falling, regional osteopenia, and impaired bone quality, contributes to the increased fracture risk. Drugs for the treatment of T2DM may also impact on the risk for fractures. For example, thiazolidinediones accelerate bone loss and increase the risk of fractures, particularly in older women. In contrast, metformin and sulfonylureas do not appear to have a negative effect on bone health and may, in fact, protect against fragility fracture. Animal models indicate a potential role for incretin hormones in bone metabolism, but there are only limited data on the impact of dipeptidyl peptidase-4 inhibitors and glucagon-like peptide-1 agonists on bone health in humans. Animal models also have demonstrated a role for amylin in bone metabolism, but clinical trials in patients with type 1 diabetes with an amylin analog (pramlintide) have not shown a significant impact on bone metabolism. The effects of insulin treatment on fracture risk are inconsistent with some studies showing an increased risk and others showing no effect. Finally, although there is limited information on the latest class of medications for the treatment of T2DM, the sodium-glucose co-transporter-2 inhibitors, these drugs do not seem to increase fracture risk. Because diabetes is an increasingly common chronic condition that can affect patients for many decades, further research into the effects of agents for the treatment of T2DM on bone metabolism is warranted. In this review, the physiological mechanism Continue reading >>

3. Metabolism Of Bone And Its Remodeling

3. Metabolism Of Bone And Its Remodeling

Bones perform many functions in a human body: 1) A mechanical function bones provide a support for muscles and protect a bone marrow 2) A reservoir of calcium and phosphates bones influence the metabolism of calcium and phosphates significantly 3) A buffer of the 3rd line bones release phosphate and bicarbonate in the long-term metabolic acidosis a) Osteoblasts and osteocytes synthesize new bone tissue a) Organic component: collagen type I and non-collagenous proteins (e.g. osteocalcin, protein S) b) Inorganic component: apatite crystallic form Ca3(PO4)2 (it can exist in a form of hydroxyapatite Ca10(PO4)6(OH)2, carbonate apatite Ca10(PO4)6CO3 or fluorapatite Ca10(PO4)6F2) Osteoblasts originate from mesenchymal cells of bone marrow. They exhibit high proteosynthetic activity and are rich in alkaline phosphatase. Their membranes contain receptors for PTH, calcitriol, growth factors, estrogens etc. and also mechanoreceptors. Their primary function is bone matter formation, bone mineralization and management of maturation and activity of osteoclasts. Osteoclasts are formed from hematopoietic cells (monocyte macrophage lineage). They contain lysosomes filled proteolytic enzymes (collagenase, gelatinase, cathepsins) and acid phosphatase isoenzyme. Membrane of osteoclasts contains a proton pump (it is able to decrease pH = 7 to pH = 4) and selected receptors (e.g. for calcitonin). Osteoclast activity but at the same time is controlled by signals from osteoblasts. Their primary function is bone resorption (runs parallel to an increased calcemia). Throughout life bone remodeling occurs continuously. It is very important because it allows the adaptation of form and organized structure of bones to biomechanical forces, maintaining the integrity of bone (repair microtraumas) and Continue reading >>

Effect Of Gh/igf-1 On Bone Metabolism And Osteoporsosis

Effect Of Gh/igf-1 On Bone Metabolism And Osteoporsosis

Effect of GH/IGF-1 on Bone Metabolism and Osteoporsosis 1Department of Health Sciences, School of Medicine, University of Milano Bicocca, Milan, Italy 2Endocrinology Department, Area Vasta N. 1, Cagli, Italy Received 13 March 2014; Revised 17 June 2014; Accepted 18 June 2014; Published 23 July 2014 Copyright 2014 Vittorio Locatelli and Vittorio E. Bianchi. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. Growth hormone (GH) and insulin-like growth factor (IGF-1) are fundamental in skeletal growth during puberty and bone health throughout life. GH increases tissue formation by acting directly and indirectly on target cells; IGF-1 is a critical mediator of bone growth. Clinical studies reporting the use of GH and IGF-1 in osteoporosis and fracture healing are outlined. Methods. A Pubmed search revealed 39 clinical studies reporting the effects of GH and IGF-1 administration on bone metabolism in osteopenic and osteoporotic human subjects and on bone healing in operated patients with normal GH secretion. Eighteen clinical studies considered the effect with GH treatment, fourteen studies reported the clinical effects with IGF-1 administration, and seven related to the GH/IGF-1 effect on bone healing. Results. Both GH and IGF-1 administration significantly increased bone resorption and bone formation in the most studies. GH/IGF-1 administration in patients with hip or tibial fractures resulted in increased bone healing, rapid clinical improvements. Some conflicting results were evidenced. Conclusions. GH and IGF-1 therapy has a significant anabolic effect. GH administration for the treatment of ost Continue reading >>

Insulin, Osteoblasts, And Energy Metabolism: Why Bone Counts Calories

Insulin, Osteoblasts, And Energy Metabolism: Why Bone Counts Calories

Insulin, osteoblasts, and energy metabolism: why bone counts calories Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. Baltimore Veterans Administration Medical Center, Baltimore, Maryland, USA. Address correspondence to: Thomas L. Clemens, Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, 601 N. Caroline St., Baltimore, Maryland 21287, USA. Phone: 410.955.3245; Fax: 410.614.1451; E-mail: [email protected] . Author information Copyright and License information Disclaimer Copyright 2014, American Society for Clinical Investigation See the article " Bone-specific insulin resistance disrupts whole-body glucose homeostasis via decreased osteocalcin activation " in volume 124 onpage1781. This article has been cited by other articles in PMC. Recent studies have demonstrated that insulin stimulates bone cells to produce and activate osteocalcin, an endocrine hormone that increases the efficiency of glucose metabolism through its actions on the pancreas and other peripheral tissues. In this issue of the JCI, Wei and colleagues directly explore the contribution of insulin signaling in osteoblasts to the disturbances in whole-body glucose metabolism associated with a high-fat diet. In mice fed a high-fat diet, increased uptake of saturated fatty acids by the osteoblast accelerates the ubiquitination and degradation of the insulin receptor. In this setting, impairments in osteoblast insulin signaling reduce serum levels of undercarboxylated osteocalcin, which in turn exacerbate insulin resistance in muscle and white adipose tissue. These findings underscore the importance of insulin-responsive skeletal cells as components of a newly appreciated endocrine network critical for regulating global e Continue reading >>

The Relationship Between Bone Turnover And Insulin Sensitivity And Secretion: Cross-sectional And Prospective Data From The Risc Cohort Study - Sciencedirect

The Relationship Between Bone Turnover And Insulin Sensitivity And Secretion: Cross-sectional And Prospective Data From The Risc Cohort Study - Sciencedirect

Bone turnover markers do not predict changes in insulin sensitivity assessed using OGTT Bone metabolism appears to influence insulin secretion and sensitivity, and insulin promotes bone formation in animals, but similar evidence in humans is limited. The objectives of this study are to explore if bone turnover markers were associated with insulin secretion and sensitivity and to determine if bone turnover markers predict changes in insulin secretion and sensitivity. The study population encompassed 576 non-diabetic adult men with normal glucose tolerance (NGT; n=503) or impaired glucose regulation (IGR; n=73). Baseline markers of bone resorption (CTX) and formation (P1NP) were determined in the fasting state and after a 2-h hyperinsulinaemic, euglycaemic clamp. An intravenous glucose tolerance test (IVGTT) and a 2-h oral glucose tolerance test (OGTT) were performed at baseline, and the OGTT was repeated after 3years. There were no differences in bone turnover marker levels between NGT and IGR. CTX and P1NP levels decreased by 8.0% (p<0.001) and 1.9% (p<0.01) between baseline and steady-state during the clamp. Fasting plasma glucose was inversely associated with CTX and P1NP both before and after adjustment for recruitment centre, age, BMI, smoking and physical activity. However, baseline bone turnover markers were neither associated with insulin sensitivity (assessed using hyperinsulinaemic euglycaemic clamp and OGTT) nor with insulin secretion capacity (based on IVGTT and OGTT) at baseline or at follow-up. Although inverse associations between fasting glucose and markers of bone turnover were identified, this study cannot support an association between insulin secretion and sensitivity in healthy, non-diabetic men. Continue reading >>

Is Insulin An Anabolic Agent In Bone? Dissecting The Diabetic Bone For Clues

Is Insulin An Anabolic Agent In Bone? Dissecting The Diabetic Bone For Clues

IN A RECENT REVIEW by Riggs and Parfitt (94) the authors propose specific criteria for classifying an agent, be it drug or hormone, as an anabolic agent for bone. They provide the following definition: [An anabolic drug] increases bone strength by increasing bone mass substantially as a result of an overall increase in bone remodeling [more BMUs (bone multicellular units) are formed] combined with a positive BMU balance (the magnitude of the formation phase is more than that of the resorption phase). Although some anabolic drugs also may induce renewed modeling, increased periosteal apposition, and repair of trabecular microstructure, these are not required properties. In this review, we will evaluate the literature to apply these criteria to insulin to determine whether this hormone is indeed an anabolic agent in bone. Insulinopenia as occurs in type 1 diabetes (T1DM) or resistance to the metabolic actions of insulin as occurs in type 2 diabetes (T2DM), are both associated with several deleterious consequences for skeletal health. Skeletal defects that are observed in conjunction with T1DM include 1) diminished linear bone growth during the pubertal growth spurt in adolescents with diabetes, 2) decreased adult bone density, 3) an increased risk for adult osteoporosis, 4) an increased risk of fragility fracture, and 5) poor bone healing and regeneration characteristics. In contrast, T2DM, a state of hyperinsulinemia and insulin resistance, is typically associated with increased bone density, yet seemingly decreased bone strength contributing again to an increased risk of fracture. Recognizing that these two clinical entities are typically characterized by differences in insulin secretion, insulin sensitivity, and/or exogenous insulin administration, we present a review Continue reading >>

Protein Supplements Increase Serum Insulin-like Growth Factor-i Levels And Attenuate Proximal Femur Bone Loss In Patients With Recent Hip Fracture: A Randomized, Double-blind, Placebo-controlled Trial

Protein Supplements Increase Serum Insulin-like Growth Factor-i Levels And Attenuate Proximal Femur Bone Loss In Patients With Recent Hip Fracture: A Randomized, Double-blind, Placebo-controlled Trial

Author, Article, and Disclosure Information Copyright 2004 by the American College of Physicians For author affiliations and current author addresses, see end of text.Grant Support: By grants from Sandoz Nutrition Ltd., Berne, Switzerland, and the Swiss National Research Science Foundation (grant no. 32-32415.91). Skin-test antigens for cellular hypersensitivity systems were supplied by Rhone-Poulenc, Thalwil, Switzerland.Acknowledgments: The authors thank M.N. Cerutti, RN, for devoted care of the patients; M. Jackson, RN, for help with patient recruitment; the staff of the osteodensitometry unit of Geneva University Hospital; G. Fourticq for muscle strength assessment; J.-L. Nussbaum for performing radiography; G. Rapatz (Institute for Medical Outcome Research) for statistical analysis; M. Perez for secretarial assistance; and E. White, MD, for reading the manuscript. They also thank J.-M. Dayer, MD; C.-H. Rapin, MD; J.-P. Michel, MD; H. Vasey, MD; P.D. Delmas, MD, PhD; and H. Schneider, PhD, for helpful discussion and support.Requests for Reprints: Rene Rizzoli, MD, Division of Bone Diseases, Department of Internal Medicine, University Hospital, CH-1211 Geneva 14, Switzerland; e-mail [email protected] Author Addresses: Drs. Schurch, Rizzoli, and Bonjour: Division of Bone Diseases, World Health Organization Collaborating Center for Osteoporosis and Bone Disease, Department of Internal Medicine, University Hospital, CH-1211 Geneva 14, Switzerland. To investigate whether oral protein supplements benefit bone metabolism in patients with recent hip fracture. 6-month, randomized, double-blind, placebo-controlled trial with a 6-month post-treatment follow-up. 82 patients (mean age, 80.7 7.4 years) with recent osteoporotic hip fracture. Patients received calcium s Continue reading >>

Insulin And Bone: Recent Developments

Insulin And Bone: Recent Developments

We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. While insulin-like growth factor I is a well-known anabolic agent in bone evidence is beginning to accumulate that its homologue, insulin, also has some anabolic properties for bone. There is specific evidence that insulin may work to stimulate osteoblast differentiation, which in turn would enhance production of osteocalcin, the osteoblast-produced peptide that can stimulate pancreatic cell proliferation and skeletal muscle insulin sensitivity. It is uncertain whether insulin stimulates bone directly or indirectly by increasing muscle work and therefore skeletal loading. We raise the question of the sequence of events that occurs with insulin resistance, such as type 2 diabetes. Evidence to date suggests that these patients have lower serum concentrations of osteocalcin, perhaps reduced skeletal loading, and reduced bone strength as evidenced by micro-indentation studies. Keywords: Type 2 diabetes, Insulin, Bone, Osteoblasts, Insulin resistance Core tip: This is a review of recent publications that suggest an anabolic loop among bone, pancreas, and skeletal muscle. The interactions between insulin and bone would on the surface appear to be an unlikely subject for an article, let alone a review article, but with the advent of the knockout mouse model many relationships that would not have been obvious now require investigation. The aim of this paper is to provide evidence supportin Continue reading >>

6 Bone Physiology | A Strategy For Research In Space Biology And Medicine In The New Century | The National Academies Press

6 Bone Physiology | A Strategy For Research In Space Biology And Medicine In The New Century | The National Academies Press

One of the best-documented pathophysiological changes associated with microgravity and the spaceflight environment is bone loss. The reduction in bone mass and its effect following reentry could substantially limit long-term human exploration of space. The development of effective countermeasures through better scientific understanding of this phenomenon is therefore essential for future crewed flights. This chapter very briefly reviews the functions of bone, bone growth and development, the process of bone remodeling (which underlies its physiological function), and the effects of hormones on this process. It summarizes current information on mechanical effects on bone, effects that may be the basis for the changes observed in microgravity or space environment conditions, briefly reviewing clinical observations; experiments on humans, animals, and cells; and putative mechanisms. It also summarizes spaceflight effects on the skeleton in humans and animals and gives caveats for these data. It then presents open questions and directions for future research aimed at continuing to characterize and understand, at a fundamental level, microgravity or space-environment-related bone loss and at developing effective countermeasures. Bone Functions, Growth And Development, And Remodeling Bone has four major functions: (1) mechanical, including support of soft tissues and locomotion; (2) storage of ions and ion homeostasis; (3) housing of the bone marrow and support of hemopoiesis; and (4) protection of the central nervous system. By fulfilling these functions, the mineralized skeleton played a central role in the evolution of terrestrial vertebrates. Suggested Citation:"6 Bone Physiology." National Research Council. 1998. A Strategy for Research in Space Biology and Medicine in Continue reading >>

Bone And Joint Problems Associated With Diabetes

Bone And Joint Problems Associated With Diabetes

If you have diabetes, you're at increased risk of various bone and joint disorders. Certain factors, such as nerve damage (diabetic neuropathy), arterial disease and obesity, may contribute to these problems — but often the cause isn't clear. Learn more about various bone and joint disorders, including symptoms and treatment options. Charcot joint What is it? Charcot (shahr-KOH) joint, also called neuropathic arthropathy, occurs when a joint deteriorates because of nerve damage — a common complication of diabetes. Charcot joint primarily affects the feet. What are the symptoms? You might have numbness and tingling or loss of sensation in the affected joints. They may become warm, red and swollen and become unstable or deformed. The involved joint may not be very painful despite its appearance. How is it treated? If detected early, progression of the disease can be slowed. Limiting weight-bearing activities and use of orthotic supports to the affected joint and surrounding structures can help. Diabetic hand syndrome What is it? Diabetic hand syndrome, also called diabetic cheiroarthropathy, is a disorder in which the skin on the hands becomes waxy and thickened. Eventually finger movement is limited. What causes diabetic hand syndrome isn't known. It's most common in people who've had diabetes for a long time. What are the symptoms? You may be unable to fully extend your fingers or press your palms together flat. How is it treated? Better management of blood glucose levels and physical therapy can slow the progress of this condition, but the limited mobility may not be reversible. Osteoporosis What is it? Osteoporosis is a disorder that causes bones to become weak and prone to fracture. People who have type 1 diabetes have an increased risk of osteoporosis. What are Continue reading >>

Insulin Resistance Linked To Lower Bone Density

Insulin Resistance Linked To Lower Bone Density

Insulin resistance linked to lower bone density (Reuters Health) - Decreasing sensitivity to insulin - often associated with obesity and eventual type 2 diabetes - may also cause young adults to have lower bone mass at a time of life when it should be at its peak, Korean researchers say. With insulin resistance, the body is less effective at using the hormone to get blood sugar into cells for energy, which leads to rising insulin levels. About 40 percent of bone mass is developed by the late teens, 90 percent by age 18 and peak lifetime bone mass is reached by the late 20s, the study team notes in the journal PLoS One. Based on a large national survey and physical exams of thousands of men and women aged 25 to 35 years old, Dr. Min Soo Choo of the Mallum University Medical Center in Seoul and colleagues found that the people with the highest levels of insulin resistance had lower bone density than those with healthier insulin processing. In order for the body to be able to handle the sugar, we need to produce more and more insulin, said Dr. Vafa Tabatabaie who wasnt involved in the study. As time goes by, insulin resistance can get worse and it can lead to prediabetes and then type 2 diabetes. That happens when essentially the body fails to keep up with increasing need for insulin, said Tabatabaie, an endocrinologist at Montefiore Health System in New York. The new study is interesting, Tabatabaie said in a phone interview, because it suggests that the effect of obesity and insulin resistance and metabolic syndrome on bone health might not just be limited to later life, which is usually when we start worrying about bone health in older people, but that it actually might start much earlier when people are expected to gain bone during their growth and maturation. Informa Continue reading >>

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