Cutaneous expression of calcium/calmodulin-dependent protein kinase II in rats with type 1 and type 2 diabetes

Matija Boric1, Antonia Jelicic Kadic1, Livia Puljak1

  • 1Laboratory for Pain Research, University of Split School of Medicine, Soltanska 2, 21000 Split, Croatia.

Insights

Calcium-calmodulin protein kinase II (CaMKII) expression increased in the skin of rats with type 1 diabetes after two months. This finding suggests CaMKII may contribute to skin changes in diabetes.

Area of Science:

  • Biochemistry
  • Dermatology
  • Endocrinology

Background:

  • Calcium-calmodulin protein kinase II (CaMKII) alterations are noted in nervous tissue of diabetic animal models.
  • Skin, sharing ectodermal origins with nervous tissue, is frequently affected in diabetic patients.

Purpose of the Study:

  • To investigate the expression patterns of CaMKII in rat skin following the induction of type 1 and type 2 diabetes.
  • To analyze CaMKII expression at two weeks and two months post-diabetes induction.

Main Methods:

  • Induction of type 1 diabetes (DM1) using streptozotocin (STZ) and type 2 diabetes (DM2) using a high-fat diet and low-dose STZ in Sprague-Dawley rats.
  • Skin samples from the plantar surface of hind paws were collected at two weeks and two months.
  • Immunohistochemistry was employed to detect total CaMKII (tCaMKII) and its alpha isoform (pCaMKIIα), with PGP 9.5 used for intraepidermal nerve fibers.

Main Results:

  • CaMKII was expressed in the epidermis of both diabetic models, with tCaMKII uniformly distributed and pCaMKIIα localized to the stratum granulosum.
  • No significant differences in tCaMKII and pCaMKIIα expression were observed at two weeks post-diabetes induction.
  • A significant increase in epidermal tCaMKII and pCaMKIIα expression was noted in DM1 animals at two months, but not in DM2 animals.

Conclusions:

  • This study provides the first description of cutaneous CaMKII expression in a diabetic model.
  • CaMKII may play a role in skin layer transformation and contribute to diabetic cutaneous changes.
  • Further research is warranted to elucidate the physiological role of CaMKII in skin and its involvement in diabetic complications.

Related Concept Videos

Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
7
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
6
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular...
23
Type I Diabetes III: Clinical Manifestations01:19

Type I Diabetes III: Clinical Manifestations

Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the...
12
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

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.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
4.8K
Diabetes Mellitus: Type 2 and Gestational01:22

Diabetes Mellitus: Type 2 and Gestational

Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
4.8K