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Article: Familial Hyperlipidemia Caused by Apolipoprotein B Mutation in the Pediatric Amish Population: A Mini Review.

Snyder, Corey / Beitelshees, Amber L / Chowdhury, Devyani

2023 Volume 15, Issue Suppl 17, Page(s) 433–437

Abstract: Familial Hypercholesterolemia (FH) is an autosomal dominant genetic disorder that causes increased low density lipoprotein cholesterol (LDL-C) levels and a higher risk of premature atherosclerosis and cardiovascular disease (CVD). Common causes of FH ... ...

Abstract	Familial Hypercholesterolemia (FH) is an autosomal dominant genetic disorder that causes increased low density lipoprotein cholesterol (LDL-C) levels and a higher risk of premature atherosclerosis and cardiovascular disease (CVD). Common causes of FH include inherited genetic mutations in the
Language	English
Publishing date	2023-07-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2537202-6
ISSN	1755-5310 ; 1755-5302
ISSN (online)	1755-5310
ISSN	1755-5302
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Critical Role for 24-Hydroxylation in Homeostatic Regulation of Vitamin D Metabolism.

Yazdi, Zhinous Shahidzadeh / Streeten, Elizabeth A / Whitlatch, Hilary B / Montasser, May E / Beitelshees, Amber L / Taylor, Simeon I

medRxiv : the preprint server for health sciences

2024

Abstract: Context: The body has evolved homeostatic mechanisms to maintain free levels of Ca: Objective: To investigate mechanisms of homeostatic regulation of vitamin D (VitD) metabolism and to apply mechanistic insights to improve clinical assessment of VitD ...

Abstract	Context: The body has evolved homeostatic mechanisms to maintain free levels of Ca Objective: To investigate mechanisms of homeostatic regulation of vitamin D (VitD) metabolism and to apply mechanistic insights to improve clinical assessment of VitD status. Design: Crossover clinical trial studying participants before and after VitD3-supplementation. Setting: Community. Participants: 11 otherwise healthy individuals with VitD-deficiency (25-hydroxyvitamin D [25(OH)D] ≤20 ng/mL). Interventions: VitD3-supplements (50,000 IU once or twice a week depending on BMI, for 4-6 weeks) were administered to achieve 25(OH)D≥30 ng/mL. Results: VitD3-supplementation significantly increased mean 25(OH)D by 2.7-fold and 24,25-dihydroxyvitamin D [24,25(OH) Conclusions: Suppression of 24-hydroxylase provides a first line of defense against symptomatic VitD-deficiency by decreasing metabolic clearance of 1,25(OH)
Language	English
Publishing date	2024-03-07
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.06.27.23291942
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Article: Vitamin D deficiency increases vulnerability to canagliflozin-induced adverse effects on 1,25-dihydroxyvitamin D and PTH.

Yazdi, Zhinous Shahidzadeh / Streeten, Elizabeth A / Whitlatch, Hilary B / Montasser, May E / Beitelshees, Amber L / Taylor, Simeon I

medRxiv : the preprint server for health sciences

2023

Abstract: Context. ...

Abstract	Context.
Language	English
Publishing date	2023-08-28
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.11.23289854
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Article ; Online: Critical Role for 24-Hydroxylation in Homeostatic Regulation of Vitamin D Metabolism.

Shahidzadeh Yazdi, Zhinous / Streeten, Elizabeth A / Whitlatch, Hilary B / Montasser, May E / Beitelshees, Amber L / Taylor, Simeon I

The Journal of clinical endocrinology and metabolism

2024

Abstract: Context: The body has evolved homeostatic mechanisms to maintain free levels of Ca+2 and 1,25-dihydroxyvitamin D [1,25(OH)2D] within narrow physiological ranges. Clinical guidelines emphasize important contributions of PTH in maintaining this ... ...

Abstract	Context: The body has evolved homeostatic mechanisms to maintain free levels of Ca+2 and 1,25-dihydroxyvitamin D [1,25(OH)2D] within narrow physiological ranges. Clinical guidelines emphasize important contributions of PTH in maintaining this homeostasis. Objective: To investigate mechanisms of homeostatic regulation of vitamin D (VitD) metabolism and to apply mechanistic insights to improve clinical assessment of VitD status. Design: Crossover clinical trial studying participants before and after VitD3-supplementation. Setting: Community. Participants: 11 otherwise healthy individuals with VitD-deficiency (25-hydroxyvitamin D [25(OH)D] ≤20 ng/mL). Interventions: VitD3-supplements (50,000 IU once or twice a week depending on BMI, for 4-6 weeks) were administered to achieve 25(OH)D≥30 ng/mL. Results: VitD3-supplementation significantly increased mean 25(OH)D by 2.7-fold and 24,25-dihydroxyvitamin D [24,25(OH)2D] by 4.3-fold. In contrast, mean levels of PTH, FGF23, and 1,25(OH)2D did not change. Mathematical modeling suggested that 24-hydroxylase activity was maximal for 25(OH)D≥50 ng/mL and achieved a minimum (∼90% suppression) with 25(OH)D<10-20 ng/mL. The 1,25(OH)2D/24,25(OH)2D ratio better predicted modeled 24-hydroxylase activity (h) (ρ=-0.85; p=0.001) compared to total plasma 25(OH)D (ρ=0.51; p=0.01) and the 24,25(OH)2D/25(OH)D ratio (ρ=0.37; p=0.3). Conclusions: Suppression of 24-hydroxylase provides a first line of defense against symptomatic VitD-deficiency by decreasing metabolic clearance of 1,25(OH)2D. The 1,25(OH)2D/24,25(OH)2D ratio provides a useful index of VitD status since it incorporates 24,25(OH)2D levels and therefore, provides insight into 24-hydroxylase activity. When VitD availability is limited, this suppresses 24-hydroxylase activity - thereby decreasing the level of 24,25(OH)2D and increasing the 1,25(OH)2D/24,25(OH)2D ratio. Thus, an increased 1,25(OH)2D/24,25(OH)2D ratio signifies triggering of homeostatic regulation, which occurs at early stages of VitD-deficiency.
Language	English
Publishing date	2024-03-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgae156
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Article ; Online: Pharmacological treatment of hyperglycemia in type 2 diabetes.

Taylor, Simeon I / Yazdi, Zhinous Shahidzadeh / Beitelshees, Amber L

The Journal of clinical investigation

2021 Volume 131, Issue 2

Abstract: Diabetes mellitus is a major public health problem, affecting about 10% of the population. Pharmacotherapy aims to protect against microvascular complications, including blindness, end-stage kidney disease, and amputations. Landmark clinical trials have ... ...

Abstract	Diabetes mellitus is a major public health problem, affecting about 10% of the population. Pharmacotherapy aims to protect against microvascular complications, including blindness, end-stage kidney disease, and amputations. Landmark clinical trials have demonstrated that intensive glycemic control slows progression of microvascular complications (retinopathy, nephropathy, and neuropathy). Long-term follow-up has demonstrated that intensive glycemic control also decreases risk of macrovascular disease, albeit rigorous evidence of macrovascular benefit did not emerge for over a decade. The US FDA's recent requirement for dedicated cardiovascular outcome trials ushered in a golden age for understanding the clinical profiles of new type 2 diabetes drugs. Some clinical trials with sodium-glucose cotransporter-2 (SGLT2) inhibitors and glucagon-like peptide 1 (GLP1) receptor agonists reported data demonstrating cardiovascular benefit (decreased risk of major adverse cardiovascular events and hospitalization for heart failure) and slower progression of diabetic kidney disease. This Review discusses current guidelines for use of the 12 classes of drugs approved to promote glycemic control in patients with type 2 diabetes. The Review also anticipates future developments with potential to improve the standard of care: availability of generic dipeptidylpeptidase-4 (DPP4) inhibitors and SGLT2 inhibitors; precision medicine to identify the best drugs for individual patients; and new therapies to protect against chronic complications of diabetes.
MeSH term(s)	Diabetes Complications/drug therapy ; Diabetes Complications/metabolism ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/pathology ; Dipeptidyl-Peptidase IV Inhibitors/therapeutic use ; Glucagon-Like Peptide-1 Receptor/agonists ; Glucagon-Like Peptide-1 Receptor/metabolism ; Glycemic Control ; Heart Failure/drug therapy ; Heart Failure/etiology ; Heart Failure/metabolism ; Humans ; Hyperglycemia/drug therapy ; Hyperglycemia/pathology ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use
Chemical Substances	Dipeptidyl-Peptidase IV Inhibitors ; GLP1R protein, human ; Glucagon-Like Peptide-1 Receptor ; Sodium-Glucose Transporter 2 Inhibitors
Language	English
Publishing date	2021-01-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI142243
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Article: Acute pharmacodynamic responses to sitagliptin: Drug-induced increase in early insulin secretion in oral glucose tolerance test.

Beitelshees, Amber L / Streeten, Elizabeth A / Yazdi, Zhinous Shahidzadeh / Whitlatch, Hilary B / Mitchell, Braxton D / Shuldiner, Alan R / Montasser, May E / Taylor, Simeon I

medRxiv : the preprint server for health sciences

2023

Abstract: ... 0.05 to 1.62+/-0.36 mU/L (p=0.04). The magnitude of sitagliptin's effect on insulin secretion ...

Abstract	Aim: DPP4 inhibitors are widely prescribed as treatments for type 2 diabetes. Because drug responses vary among individuals, we initiated investigations to identify genetic variants associated with the magnitude of drug responses. Methods: Sitagliptin (100 mg) was administered to 47 healthy volunteers. Several endpoints were measured to assess clinically relevant responses - including the effect of sitagliptin on glucose and insulin levels during an oral glucose tolerance test (OGTT). Results: This pilot study confirmed that sitagliptin (100 mg) decreased the area under the curve for glucose during an OGTT (p=0.0003). Furthermore, sitagliptin promoted insulin secretion during the early portion of the OGTT as reflected by an increase in the ratio of plasma insulin at 30 min divided by plasma insulin at 60 min (T30:T60) from 0.87+/-0.05 to 1.62+/-0.36 mU/L (p=0.04). The magnitude of sitagliptin's effect on insulin secretion (as judged by the increase in the T30:T60 ratio for insulin) was correlated with the magnitude of sitagliptin-induced increase in the area under the curve for intact plasma GLP1 levels during the first hour of the OGTT. This study confirmed previously reported sex differences in glucose and insulin levels during an OGTT. Specifically, females exhibited higher levels of glucose and insulin at the 90-180 min time points. However, we did not detect significant sex-associated differences in the magnitude of sitagliptin-induced changes in T30:T60 ratios for either glucose or insulin. Conclusions: T30:T60 ratios for insulin and glucose during an OGTT provide useful indices to assess pharmacodynamic responses to DPP4 inhibitors.
Language	English
Publishing date	2023-10-19
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.09.24.23296026
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Vitamin D Deficiency Increases Vulnerability to Canagliflozin-induced Adverse Effects on 1,25-Dihydroxyvitamin D and PTH.

Shahidzadeh Yazdi, Zhinous / Streeten, Elizabeth A / Whitlatch, Hilary B / Montasser, May E / Beitelshees, Amber L / Taylor, Simeon I

The Journal of clinical endocrinology and metabolism

2023 Volume 109, Issue 2, Page(s) e646–e656

Abstract: Context: Canagliflozin has been reported to increase the risk of bone fracture-possibly mediated by decreasing 1,25-dihydroxyvitamin D (1,25(OH)2D) and increasing parathyroid hormone (PTH).: Objective: This work investigated whether baseline vitamin ... ...

Abstract	Context: Canagliflozin has been reported to increase the risk of bone fracture-possibly mediated by decreasing 1,25-dihydroxyvitamin D (1,25(OH)2D) and increasing parathyroid hormone (PTH). Objective: This work investigated whether baseline vitamin D (VitD) deficiency renders individuals vulnerable to this adverse effect and whether VitD3 supplementation is protective. Methods: This community-based, outpatient study had a paired design comparing individual participants before and after VitD3 supplementation. Eleven VitD-deficient (25-hydroxyvitamin D [25(OH)D] ≤ 20 ng/mL) individuals were recruited from the Amish population in Lancaster, Pennsylvania. Participants underwent 2 canagliflozin challenge protocols (300 mg daily for 5 days): the first before and the second after VitD3 supplementation. In the VitD3 supplementation protocol, participants received VitD3 supplementation (50 000 IU once or twice a week depending on body mass index for 4-6 weeks) to achieve 25(OH)D of 30 ng/mL or greater. Two coprimary end points were identified: effects of VitD3 supplementation on canagliflozin-induced changes in 1,25(OH)2D and PTH. Secondary end points included effects of VitD3 supplementation on baseline levels of VitD metabolites and PTH. Results: VitD3 supplementation increased mean 25(OH)D from 16.5 ± 1.6 to 44.3 ± 5.5 ng/mL (P = .0006) and 24,25-dihydroxyvitamin D (24,25(OH)2D) from 1.0 ± 0.1 to 4.3 ± 0.6 ng/mL (P = .0002). Mean 1,25(OH)2D and PTH were unchanged. VitD3 supplementation decreased the magnitude of canagliflozin-induced changes in 1,25(OH)2D (from -31.3%±4.7% to -9.3%±8.3%; P = .04) and PTH (from +36.2%±6.2% to +9.7%±3.7%; P = .005). Conclusion: VitD deficiency rendered individuals more vulnerable to adverse effects of canagliflozin on biomarkers associated with bone health. VitD3 supplementation was protective against canagliflozin's short-term adverse effects on 1,25(OH)2D and PTH.
MeSH term(s)	Humans ; Parathyroid Hormone ; Canagliflozin/adverse effects ; Vitamin D/metabolism ; Vitamin D Deficiency/drug therapy ; Vitamins ; Ergocalciferols ; Dietary Supplements/adverse effects
Chemical Substances	1,25-dihydroxyvitamin D (66772-14-3) ; Parathyroid Hormone ; Canagliflozin (0SAC974Z85) ; Vitamin D (1406-16-2) ; Vitamins ; Ergocalciferols
Language	English
Publishing date	2023-09-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgad554
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Article ; Online: Personalised antiplatelet treatment: a RAPIDly moving target.

Beitelshees, Amber L

Lancet (London, England)

2012 Volume 379, Issue 9827, Page(s) 1680–1682

MeSH term(s)	Angioplasty, Balloon, Coronary ; Aryl Hydrocarbon Hydroxylases/genetics ; Cytochrome P-450 CYP2C19 ; Female ; Genetic Carrier Screening ; Genetic Testing ; Humans ; Male ; Platelet Aggregation Inhibitors/therapeutic use ; Point-of-Care Systems ; Precision Medicine ; Purinergic P2Y Receptor Antagonists/therapeutic use
Chemical Substances	Platelet Aggregation Inhibitors ; Purinergic P2Y Receptor Antagonists ; Aryl Hydrocarbon Hydroxylases (EC 1.14.14.1) ; CYP2C19 protein, human (EC 1.14.14.1) ; Cytochrome P-450 CYP2C19 (EC 1.14.14.1)
Language	English
Publishing date	2012-03-29
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	3306-6
ISSN	1474-547X ; 0023-7507 ; 0140-6736
ISSN (online)	1474-547X
ISSN	0023-7507 ; 0140-6736
DOI	10.1016/S0140-6736(12)60431-0
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Article ; Online: Sodium-Glucose Cotransporter 2 Inhibitors: A Case Study in Translational Research.

Beitelshees, Amber L / Leslie, Bruce R / Taylor, Simeon I

Diabetes

2019 Volume 68, Issue 6, Page(s) 1109–1120

Abstract: Sodium-glucose cotransporter 2 (SGLT2) inhibitors are the most recently approved class of diabetes drugs. Unlike other agents, SGLT2 inhibitors act on the kidney to promote urinary glucose excretion. SGLT2 inhibitors provide multiple benefits, including ... ...

Abstract	Sodium-glucose cotransporter 2 (SGLT2) inhibitors are the most recently approved class of diabetes drugs. Unlike other agents, SGLT2 inhibitors act on the kidney to promote urinary glucose excretion. SGLT2 inhibitors provide multiple benefits, including decreased HbA
MeSH term(s)	Acute Kidney Injury/chemically induced ; Blood Pressure ; Body Weight ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism ; Fasciitis, Necrotizing/chemically induced ; Fractures, Bone/chemically induced ; Glycated Hemoglobin A/metabolism ; Humans ; Hyperkalemia/chemically induced ; Ketosis/chemically induced ; Reproductive Tract Infections/etiology ; Sodium-Glucose Transporter 2/metabolism ; Sodium-Glucose Transporter 2 Inhibitors/therapeutic use ; Translational Research, Biomedical ; Urinary Tract Infections/etiology ; Weight Loss
Chemical Substances	Glycated Hemoglobin A ; Sodium-Glucose Transporter 2 ; Sodium-Glucose Transporter 2 Inhibitors ; hemoglobin A1c protein, human
Language	English
Publishing date	2019-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/dbi18-0006
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Article ; Online: Is ticagrelor the antiplatelet therapy panacea?

Beitelshees, Amber L

Circulation. Cardiovascular genetics

2010 Volume 3, Issue 6, Page(s) 489–491

MeSH term(s)	Adenosine/analogs & derivatives ; Adenosine/therapeutic use ; Aryl Hydrocarbon Hydroxylases/genetics ; Aryl Hydrocarbon Hydroxylases/metabolism ; Clopidogrel ; Cytochrome P-450 CYP2C19 ; Humans ; Purinergic P2Y Receptor Antagonists/therapeutic use ; Ticagrelor ; Ticlopidine/analogs & derivatives ; Ticlopidine/metabolism ; Ticlopidine/therapeutic use ; Treatment Outcome
Chemical Substances	Purinergic P2Y Receptor Antagonists ; Clopidogrel (A74586SNO7) ; Aryl Hydrocarbon Hydroxylases (EC 1.14.14.1) ; CYP2C19 protein, human (EC 1.14.14.1) ; Cytochrome P-450 CYP2C19 (EC 1.14.14.1) ; Ticagrelor (GLH0314RVC) ; Adenosine (K72T3FS567) ; Ticlopidine (OM90ZUW7M1)
Language	English
Publishing date	2010-11-15
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2477394-3
ISSN	1942-3268 ; 1942-325X
ISSN (online)	1942-3268
ISSN	1942-325X
DOI	10.1161/CIRCGENETICS.110.958611
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