Teriparatide (human parathyroid hormone (1-34)) inhibits osteogenic vascular calcification in diabetic low density lipoprotein receptor-deficient mice.

Shao JS, Cheng SL, Charlton-Kachigian N, Loewy AP, Towler DA

The Journal of biological chemistry22 Sept 2003Cited by 133 (Europe PMC)

PMID14504275DOI10.1074/jbc.m308825200PepBankPUB-14504275

Summary

Cardiovascular calcification is a common consequence of diabetes. High fat diets induce diabetes and arterial calcification in male low density lipoprotein receptor (LDLR) -/- mice; calcification occurs via Msx2 signaling that promotes the osteogenic differentiation of arterial myofibroblasts. We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week. Gene expression was determined from single aortas and hind limb RNA by fluorescence reverse transcription-PCR. Valve calcification was determined by histological staining of cardiac sections using image analysis to quantify valve leaflet mineralization. PTH(1-34) increased bone mineral content (by dual energy x-ray absorptiometry) in LDLR -/- mice, with induction of osseous osteopontin (OPN) expression and serum OPN levels (>150 nM); PTH(1-34) did not significantly change serum glucose, lipids, body weight, or fat mass. PTH(1-34) suppressed aortic OPN and Msx2 expression >50% and decreased cardiac valve calcification 80% (8.3 +/- 1.5% versus 1.4 +/- 0.5%; p < 0.001). Of the known circulating regulators of vascular calcification (OPN, osteoprotegerin, and leptin), PTH(1-34) regulated only serum OPN. We therefore studied actions of PTH(1-34) and OPN in vitro on cells induced to mineralize with Msx2. OPN (5-50 nM) reversed Msx2-induced mineralization. PTH(1-34) inhibited mineralization by 40% and down-regulated Msx2 in aortic myofibroblasts. PTH(1-34) inhibits vascular calcification and aortic osteogenic differentiation via direct actions and potentially via circulating OPN. PTH(1-34) exerts beneficial actions at early stages of macrovascular disease responses to diabetes and dyslipidemia.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study14

14 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In diabetic LDLR-deficient mice, PTH increased bone mineral content.
In plain wordsIn mice with diabetes, PTH increased bone mineral content.
Peptide
Teriparatide (PTH 1-34)
Outcome
IncreaseBone mineral content
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Bone and joint · Musculoskeletal
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Source sentences
Summary
PTH(1-34) increased bone mineral content (by dual energy x-ray absorptiometry) in LDLR -/- mice,
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427501
02AnimalAnimal study (in vivo)Mechanism
In diabetic LDLR-deficient mice, PTH induced osseous osteopontin expression.
In plain wordsIn mice with diabetes, PTH increased osteopontin expression in bone.
Peptide
Teriparatide (PTH 1-34)
Outcome
IncreaseOsseous osteopontin expression
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Bone and joint · Musculoskeletal
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Source sentences
Summary
with induction of osseous osteopontin (OPN) expression and serum OPN levels (>150 nM)
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427502
03AnimalAnimal study (in vivo)Mechanism
In diabetic LDLR-deficient mice, PTH increased serum osteopontin above 150 nM.
In plain wordsIn mice with diabetes, PTH increased blood osteopontin.
Peptide
Teriparatide (PTH 1-34)
Outcome
IncreaseSerum osteopontin
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Bone and joint · Musculoskeletal
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Measurements
Serum OPN
> 150 nM
PTH-treated mice
Source sentences
Summary
with induction of osseous osteopontin (OPN) expression and serum OPN levels (>150 nM)
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427503
04AnimalAnimal study (in vivo)Efficacy outcome
In diabetic LDLR-deficient mice, PTH did not significantly change serum glucose.
In plain wordsIn mice with diabetes, PTH did not significantly change blood glucose.
Peptide
Teriparatide (PTH 1-34)
Outcome
No significant changeSerum glucose
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Glycemic control · Metabolic and weight
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Source sentences
Summary
PTH(1-34) did not significantly change serum glucose, lipids, body weight, or fat mass.
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427504
05AnimalAnimal study (in vivo)Efficacy outcome
In diabetic LDLR-deficient mice, PTH did not significantly change serum lipids.
In plain wordsIn mice with diabetes, PTH did not significantly change blood lipids.
Peptide
Teriparatide (PTH 1-34)
Outcome
No significant changeSerum lipids
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Lipids · Metabolic and weight
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Source sentences
Summary
PTH(1-34) did not significantly change serum glucose, lipids, body weight, or fat mass.
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427505
06AnimalAnimal study (in vivo)Efficacy outcome
In diabetic LDLR-deficient mice, PTH did not significantly change body weight.
In plain wordsIn mice with diabetes, PTH did not significantly change body weight.
Peptide
Teriparatide (PTH 1-34)
Outcome
No significant changeBody weight
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Body weight · Metabolic and weight
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Source sentences
Summary
PTH(1-34) did not significantly change serum glucose, lipids, body weight, or fat mass.
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427506
07AnimalAnimal study (in vivo)Efficacy outcome
In diabetic LDLR-deficient mice, PTH did not significantly change fat mass.
In plain wordsIn mice with diabetes, PTH did not significantly change fat mass.
Peptide
Teriparatide (PTH 1-34)
Outcome
No significant changeFat mass
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Body weight · Metabolic and weight
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Source sentences
Summary
PTH(1-34) did not significantly change serum glucose, lipids, body weight, or fat mass.
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427507
08AnimalAnimal study (in vivo)Mechanism
In diabetic LDLR-deficient mice, PTH suppressed aortic osteopontin expression by more than 50%.
In plain wordsIn mice with diabetes, PTH reduced osteopontin expression in the aorta.
Peptide
Teriparatide (PTH 1-34)
Outcome
DecreaseAortic osteopontin expression
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Source sentences
Summary
PTH(1-34) suppressed aortic OPN and Msx2 expression >50% and decreased cardiac valve calcification 80% (8.3 +/- 1.5% versus 1.4 +/- 0.5%; p < 0.001).
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427508
09AnimalAnimal study (in vivo)Mechanism
In diabetic LDLR-deficient mice, PTH suppressed aortic Msx2 expression by more than 50%.
In plain wordsIn mice with diabetes, PTH reduced Msx2 expression in the aorta.
Peptide
Teriparatide (PTH 1-34)
Outcome
DecreaseAortic Msx2 expression
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Source sentences
Summary
PTH(1-34) suppressed aortic OPN and Msx2 expression >50% and decreased cardiac valve calcification 80% (8.3 +/- 1.5% versus 1.4 +/- 0.5%; p < 0.001).
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427509
10AnimalAnimal study (in vivo)Efficacy outcome
In diabetic LDLR-deficient mice, PTH decreased cardiac valve calcification by 80%.
In plain wordsIn mice with diabetes, PTH reduced heart valve calcification.
Peptide
Teriparatide (PTH 1-34)
Outcome
DecreaseCardiac valve calcification
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Bone and joint · Cardiovascular
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Measurements
Calcification reduction
80%
PTH versus vehicle
Source sentences
Summary
PTH(1-34) suppressed aortic OPN and Msx2 expression >50% and decreased cardiac valve calcification 80% (8.3 +/- 1.5% versus 1.4 +/- 0.5%; p < 0.001).
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427510
11AnimalAnimal study (in vivo)Mechanism
In diabetic LDLR-deficient mice, PTH did not regulate serum osteoprotegerin.
In plain wordsIn mice with diabetes, PTH did not change blood osteoprotegerin.
Peptide
Teriparatide (PTH 1-34)
Outcome
No significant changeSerum osteoprotegerin
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Source sentences
Summary
Of the known circulating regulators of vascular calcification (OPN, osteoprotegerin, and leptin), PTH(1-34) regulated only serum OPN.
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427511
12AnimalAnimal study (in vivo)Mechanism
In diabetic LDLR-deficient mice, PTH did not regulate serum leptin.
In plain wordsIn mice with diabetes, PTH did not change blood leptin.
Peptide
Teriparatide (PTH 1-34)
Outcome
No significant changeSerum leptin
Study
mousen: not reported in source
Diabetic LDLR-deficient mice
Comparator
Vehicle
Outcome group
Receptor activity and mechanism · Metabolic and weight
Studied dose
0.4 mg/kg five times/week · subcutaneous · 4 weeksAs given in this study (mouse).
Source sentences
Summary
Of the known circulating regulators of vascular calcification (OPN, osteoprotegerin, and leptin), PTH(1-34) regulated only serum OPN.
1 context sentence(design, population, supporting numbers)
Summary · context
We studied regulation of arterial osteogenesis by human parathyroid hormone (PTH) (1-34) (also called teriparatide) in LDLR -/- mice fed diabetogenic diets for 4 weeks. LDLR -/- mice were treated with vehicle or 0.4 mg/kg of PTH(1-34) subcutaneously five times/week.
Show in the study text Report a problemFND-1450427512
13LabIn vitro (cells)Efficacy outcome
In aortic myofibroblasts, PTH inhibited mineralization by 40%.
In plain wordsIn cells, PTH reduced mineralization in aortic myofibroblasts.
Peptide
Teriparatide (PTH 1-34)
Outcome
DecreaseMineralization
Study
n: not reported in source
Aortic myofibroblasts induced to mineralize with Msx2
Outcome group
Bone and joint · Cardiovascular
Studied dose
Dose not stated
Measurements
Mineralization inhibition
40%
PTH-treated aortic myofibroblasts
Source sentences
Summary
PTH(1-34) inhibited mineralization by 40% and down-regulated Msx2 in aortic myofibroblasts.
1 context sentence(design, population, supporting numbers)
Summary · context
We therefore studied actions of PTH(1-34) and OPN in vitro on cells induced to mineralize with Msx2.
Show in the study text Report a problemFND-1450427513
14LabIn vitro (cells)Mechanism
In aortic myofibroblasts, PTH down-regulated Msx2.
In plain wordsIn cells, PTH reduced Msx2 expression in aortic myofibroblasts.
Peptide
Teriparatide (PTH 1-34)
Outcome
DecreaseMsx2 expression
Study
n: not reported in source
Aortic myofibroblasts
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
PTH(1-34) inhibited mineralization by 40% and down-regulated Msx2 in aortic myofibroblasts.
Show in the study text Report a problemFND-1450427514

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

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Version 2Current
22 Oct 2026, 02:26 UTC
Study results updated
Version 1
21 Oct 2026, 18:59 UTC
First added · source update from Europe PMC

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Teriparatide (human parathyroid hormone (1-34)) inhibits osteogenic vascular calcification in diabetic low density lipoprotein receptor-deficient mice.

Summary

Results from this study14

Version history

Subjects

Publication types

MeSH terms