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Related Concept Videos

Synthesis and Functions of Calcitonin00:51

Synthesis and Functions of Calcitonin

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Calcitonin, a vital polypeptide hormone, regulates calcium levels within body fluids. It is released by the parafollicular cells, also known as C cells, situated in the follicular epithelium of the thyroid gland. Calcitonin responds to fluctuations in blood calcium levels and the influence of gastrointestinal hormones like gastrin and cholecystokinin.
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Skeleton and Calcium Homeostasis01:21

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Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
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Aging01:26

Aging

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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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Feedback Regulation of Calcium Concentration01:27

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Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
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The Effect of Aging on Tissues01:19

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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

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Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
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Analysis of Beta-cell Function Using Single-cell Resolution Calcium Imaging in Zebrafish Islets
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Analysis of Beta-cell Function Using Single-cell Resolution Calcium Imaging in Zebrafish Islets

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β-Cell Ca(2+) dynamics and function are compromised in aging.

Christopher J Barker1, Luosheng Li1, Martin Köhler1

  • 1The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, Karolinska University Hospital L1, SE-171 76 Stockholm, Sweden.

Advances in Biological Regulation
|October 6, 2014
PubMed
Summary
This summary is machine-generated.

Aging impairs pancreatic beta-cell function by altering calcium (Ca2+) signaling, impacting insulin secretion and contributing to type 2 diabetes. Mitochondrial dysfunction plays a key role in these age-dependent changes.

Keywords:
AgingCalciumCalcium oscillationsDiabetesInsulin secretionPancreatic beta cell

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Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells
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Imaging Calcium Dynamics in Subpopulations of Mouse Pancreatic Islet Cells

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Area of Science:

  • Endocrinology
  • Cell Biology
  • Metabolic Diseases

Background:

  • Pancreatic beta-cell dysfunction is central to type 2 diabetes (T2D) pathogenesis.
  • Age-dependent decline in beta-cell function is observed, but underlying molecular mechanisms remain unclear.
  • Cytoplasmic free Ca(2+) concentration ([Ca(2+)]i) regulation, dependent on mitochondrial function, is critical for beta-cell function.

Purpose of the Study:

  • To investigate the molecular mechanisms of age-dependent deterioration in pancreatic beta-cell function.
  • To examine the role of calcium ([Ca(2+)]i) dynamics and mitochondrial function in aging beta-cells.
  • To compare aging phenotypes in different mouse models.

Main Methods:

  • Utilized three mouse models: premature aging (mitochondrial mutator), mature aging (C57BL/6), and aging-resistant (129).
  • Assessed cytoplasmic free Ca(2+) concentration ([Ca(2+)]i) dynamics in pancreatic beta-cells.
  • Investigated inositol 1,4,5-trisphosphate (Ins(1,4,5)P3)-mediated Ca(2+) mobilization and plasma membrane Ca(2+) influx.

Main Results:

  • Age-dependent mitochondrial impairment causes modest alterations in beta-cell [Ca(2+)]i dynamics, particularly affecting oscillation patterns.
  • Changes in [Ca(2+)]i dynamics are linked to modified PLC/Ins(1,4,5)P3-mediated Ca(2+) release and reduced beta-cell Ca(2+) influx.
  • Even minor, time-dependent signal transduction changes in beta-cells compromise insulin release and lead to a diabetic phenotype.

Conclusions:

  • Mitochondrial dysfunction contributes to age-dependent impairments in beta-cell calcium signaling.
  • Altered calcium dynamics in aging beta-cells disrupt insulin secretion, promoting type 2 diabetes.
  • Targeting age-related signaling pathways may offer therapeutic strategies for T2D.