CaMKK2 Signaling in Metabolism and Skeletal Disease

a New Axis with Therapeutic Potential

Justin N. Williams, Uma Sankar

Research output: Contribution to journalReview article

Abstract

Purpose of Review: Age and metabolic disorders result in the accumulation of advanced glycation endproducts (AGEs), oxidative stress, and inflammation, which cumulatively cause a decline in skeletal health. Bone becomes increasingly vulnerable to fractures and its regenerative capacity diminishes under such conditions. With a rapidly aging population in the USA and the global increase in diabetes, efficacious, multi-dimensional therapies that can treat or prevent skeletal diseases associated with metabolic dysfunction and inflammatory disorders are acutely needed. Recent Findings: Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) is a key regulator of nutrient intake, glucose metabolism, insulin production, and adipogenesis. Recent studies suggest a pivotal role for CaMKK2 in bone metabolism, fracture healing, and inflammation. Summary: Aside from rekindling previous concepts of CaMKK2 as a potent regulator of whole-body energy homeostasis, this review emphasizes CaMKK2 as a potential therapeutic target to treat skeletal diseases that underlie metabolic conditions and inflammation.

Original languageEnglish (US)
JournalCurrent Osteoporosis Reports
DOIs
StatePublished - Jan 1 2019

Fingerprint

Calcium-Calmodulin-Dependent Protein Kinases
Phosphotransferases
Inflammation
Adipogenesis
Fracture Healing
Metabolic Diseases
Bone Fractures
Therapeutics
Oxidative Stress
Homeostasis
Insulin
Bone and Bones
Glucose
Food
Health
Population

Keywords

  • CaMKK2
  • Diabetes
  • Diabetic osteopathy
  • Fracture healing
  • Skeletal disease

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism

Cite this

CaMKK2 Signaling in Metabolism and Skeletal Disease : a New Axis with Therapeutic Potential. / Williams, Justin N.; Sankar, Uma.

In: Current Osteoporosis Reports, 01.01.2019.

Research output: Contribution to journalReview article

@article{6fb15197f0224886a52ece55e12d1d58,
title = "CaMKK2 Signaling in Metabolism and Skeletal Disease: a New Axis with Therapeutic Potential",
abstract = "Purpose of Review: Age and metabolic disorders result in the accumulation of advanced glycation endproducts (AGEs), oxidative stress, and inflammation, which cumulatively cause a decline in skeletal health. Bone becomes increasingly vulnerable to fractures and its regenerative capacity diminishes under such conditions. With a rapidly aging population in the USA and the global increase in diabetes, efficacious, multi-dimensional therapies that can treat or prevent skeletal diseases associated with metabolic dysfunction and inflammatory disorders are acutely needed. Recent Findings: Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) is a key regulator of nutrient intake, glucose metabolism, insulin production, and adipogenesis. Recent studies suggest a pivotal role for CaMKK2 in bone metabolism, fracture healing, and inflammation. Summary: Aside from rekindling previous concepts of CaMKK2 as a potent regulator of whole-body energy homeostasis, this review emphasizes CaMKK2 as a potential therapeutic target to treat skeletal diseases that underlie metabolic conditions and inflammation.",
keywords = "CaMKK2, Diabetes, Diabetic osteopathy, Fracture healing, Skeletal disease",
author = "Williams, {Justin N.} and Uma Sankar",
year = "2019",
month = "1",
day = "1",
doi = "10.1007/s11914-019-00518-w",
language = "English (US)",
journal = "Current Alzheimer Research",
issn = "1546-9530",
publisher = "W.B. Saunders Ltd",

}

TY - JOUR

T1 - CaMKK2 Signaling in Metabolism and Skeletal Disease

T2 - a New Axis with Therapeutic Potential

AU - Williams, Justin N.

AU - Sankar, Uma

PY - 2019/1/1

Y1 - 2019/1/1

N2 - Purpose of Review: Age and metabolic disorders result in the accumulation of advanced glycation endproducts (AGEs), oxidative stress, and inflammation, which cumulatively cause a decline in skeletal health. Bone becomes increasingly vulnerable to fractures and its regenerative capacity diminishes under such conditions. With a rapidly aging population in the USA and the global increase in diabetes, efficacious, multi-dimensional therapies that can treat or prevent skeletal diseases associated with metabolic dysfunction and inflammatory disorders are acutely needed. Recent Findings: Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) is a key regulator of nutrient intake, glucose metabolism, insulin production, and adipogenesis. Recent studies suggest a pivotal role for CaMKK2 in bone metabolism, fracture healing, and inflammation. Summary: Aside from rekindling previous concepts of CaMKK2 as a potent regulator of whole-body energy homeostasis, this review emphasizes CaMKK2 as a potential therapeutic target to treat skeletal diseases that underlie metabolic conditions and inflammation.

AB - Purpose of Review: Age and metabolic disorders result in the accumulation of advanced glycation endproducts (AGEs), oxidative stress, and inflammation, which cumulatively cause a decline in skeletal health. Bone becomes increasingly vulnerable to fractures and its regenerative capacity diminishes under such conditions. With a rapidly aging population in the USA and the global increase in diabetes, efficacious, multi-dimensional therapies that can treat or prevent skeletal diseases associated with metabolic dysfunction and inflammatory disorders are acutely needed. Recent Findings: Ca2+/calmodulin-dependent protein kinase kinase 2 (CaMKK2) is a key regulator of nutrient intake, glucose metabolism, insulin production, and adipogenesis. Recent studies suggest a pivotal role for CaMKK2 in bone metabolism, fracture healing, and inflammation. Summary: Aside from rekindling previous concepts of CaMKK2 as a potent regulator of whole-body energy homeostasis, this review emphasizes CaMKK2 as a potential therapeutic target to treat skeletal diseases that underlie metabolic conditions and inflammation.

KW - CaMKK2

KW - Diabetes

KW - Diabetic osteopathy

KW - Fracture healing

KW - Skeletal disease

UR - http://www.scopus.com/inward/record.url?scp=85066915274&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85066915274&partnerID=8YFLogxK

U2 - 10.1007/s11914-019-00518-w

DO - 10.1007/s11914-019-00518-w

M3 - Review article

JO - Current Alzheimer Research

JF - Current Alzheimer Research

SN - 1546-9530

ER -