The Effect of Pramlintide (Amylin Analogue) Treatment on Bone Metabolism and Bone Density in Patients with Type 1 Diabetes Mellitus

Borm, Anne Katrin; Klevesath, M. S.; Borcea, V.; Kasperk, C.; Seibel, Markus J.; Wahl, Peter; Ziegler, Reinhard; Nawroth, PP

doi:10.1055/s-2007-978777

Cited by 30 publications

(11 citation statements)

References 11 publications

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“…There was no statistically significant change in BMD or markers of bone metabolism after 1 year. The subjects did not have osteopenia at baseline, and therefore the impact of pramlintide on bone metabolism in patients with T1DM and osteopenia is unclear (137).…”

Section: Results From Clinical Trialsmentioning

confidence: 99%

“…The impact of pramlintide on bone metabolism has not been extensively studied. Borm et al (137) conducted a small clinical trial in 23 patients (13 males and 10 females) with T1DM (age, 42.2 Ϯ 10.3 y; duration of diabetes, 20.7 Ϯ 9.8 y) that investigated the effect of 12 months of treatment with pramlintide on bone metabolism. BMD measurement of the lumbar spine by dual-energy x-ray absorptiometry and biochemical markers of bone metabolism, including calcium, PTH, osteocalcin, and urinary pyridinium crosslinks, were obtained at baseline and after 1 year of treatment with pramlintide.…”

Section: Results From Clinical Trialsmentioning

confidence: 99%

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The Impact of Diabetes and Diabetes Medications on Bone Health

2015

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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 mechanisms and clinical impact of diabetes treatments on bone health and fracture risk in patients with T2DM are described.

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Section: Results From Clinical Trialsmentioning

confidence: 99%

Section: Results From Clinical Trialsmentioning

confidence: 99%

The Impact of Diabetes and Diabetes Medications on Bone Health

2015

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“…However, only one study has directly examined the skeletal effects of pramlintide therapy in humans. In a study of 23 non‐osteoporotic T1D patients (mean age ~45 years; mean duration of T1D ~21 years), 12 months of treatment with pramlintide, as four injections per day, did not impart a significant change in BMD, or in bone biomarkers (calcium, PTH, osteocalcin, pyridinium cross‐links) after 1 year . However, because these subjects were not osteoporotic at baseline, the implication of these findings may be limited; moreover, they do not provide any evidence of the impact of pramlintide on fracture risk, specifically.…”

Section: Drugs and Bonementioning

confidence: 93%

Diabetes pharmacotherapy and effects on the musculoskeletal system

Kalaitzoglou

Fowlkes

Popescu

et al. 2018

Diabetes Metabolism Res

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Summary Persons with type 1 or type 2 diabetes have a significantly higher fracture risk than age‐matched persons without diabetes, attributed to disease‐specific deficits in the microarchitecture and material properties of bone tissue. Therefore, independent effects of diabetes drugs on skeletal integrity are vitally important. Studies of incretin‐based therapies have shown divergent effects of different agents on fracture risk, including detrimental, beneficial, and neutral effects. The sulfonylurea class of drugs, owing to its hypoglycemic potential, is thought to amplify the risk of fall‐related fractures, particularly in the elderly. Other agents such as the biguanides may, in fact, be osteo‐anabolic. In contrast, despite similarly expected anabolic properties of insulin, data suggests that insulin pharmacotherapy itself, particularly in type 2 diabetes, may be a risk factor for fracture, negatively associated with determinants of bone quality and bone strength. Finally, sodium‐dependent glucose co‐transporter 2 inhibitors have been associated with an increased risk of atypical fractures in select populations, and possibly with an increase in lower extremity amputation with specific SGLT2I drugs. The role of skeletal muscle, as a potential mediator and determinant of bone quality, is also a relevant area of exploration. Currently, data regarding the impact of glucose lowering medications on diabetes‐related muscle atrophy is more limited, although preclinical studies suggest that various hypoglycemic agents may have either aggravating (sulfonylureas, glinides) or repairing (thiazolidinediones, biguanides, incretins) effects on skeletal muscle atrophy, thereby influencing bone quality. Hence, the therapeutic efficacy of each hypoglycemic agent must also be evaluated in light of its impact, alone or in combination, on musculoskeletal health, when determining an individualized treatment approach. Moreover, the effect of newer medications (potentially seeking expanded clinical indication into the pediatric age range) on the growing skeleton is largely unknown. Herein, we review the available literature regarding effects of diabetes pharmacotherapy, by drug class and/or by clinical indication, on the musculoskeletal health of persons with diabetes.

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“…In addition, the study found that women with anorexia nervosa had significantly lower levels of fasting amylin, suggesting that amylin could be one of the mechanisms underlying bone loss in anorexia nervosa (85). In another study, a group of patients with type 1 diabetes were treated with pramlintide (amylin analog) for 12 months (86). Although these patients were expected to benefit from the therapy due to the chronic amylin deficiency associated with diabetes, no change in BMD or biochemical markers of bone metabolism was observed following the treatment.…”

Section: Beta-pancreatic Hormonesmentioning

confidence: 99%

Cytokines and Hormones That Contribute to the Positive Association between Fat and Bone

Naot

Cornish

2014

Front. Endocrinol.

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The positive association between body weight and bone density has been established in numerous laboratory and clinical studies. Apart from the direct effect of soft tissue mass on bone through skeletal loading, a number of cytokines and hormones contribute to the positive association between adipose and bone tissue, acting either locally in sites where cells of the two tissues are adjacent to each other or systemically through the circulation. The current review describes the effects of such local and systemic factors on bone physiology. One class of factors are the adipocyte-secreted peptides (adipokines), which affect bone turnover through a combination of direct effects in bone cells and indirect mechanisms mediated by the central nervous system. Another source of hormones that contribute to the coupling between fat and bone tissue are beta cells of the pancreas. Insulin, amylin, and preptin are co-secreted from pancreatic beta cells in response to increased glucose levels after feeding, and are also found in high circulating levels in obesity. A number of peptide hormones secreted from the gastrointestinal tract in response to feeding affect both fat and bone cells and thus can also act as mediators of the association between the two tissues. The current review focuses on results of laboratory studies investigating possible mechanism involved in the positive association between fat mass and bone mass.

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The Effect of Pramlintide (Amylin Analogue) Treatment on Bone Metabolism and Bone Density in Patients with Type 1 Diabetes Mellitus

Cited by 30 publications

References 11 publications

The Impact of Diabetes and Diabetes Medications on Bone Health

The Impact of Diabetes and Diabetes Medications on Bone Health

Diabetes pharmacotherapy and effects on the musculoskeletal system

Cytokines and Hormones That Contribute to the Positive Association between Fat and Bone

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