ArticleDiabetes2012
Hyperthermia with mild electrical stimulation protects pancreatic β-cells from cell stresses and apoptosis.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06377358 (Lipolysis of Visceral Reserve Fat Using Tecar Therapy), which is not on this map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Lipolysis of Visceral Reserve Fat Using Tecar Therapy: Anthropometric, Biochemical and NMR Imaging Study.
Who cites it
21 citing papers in PubMed, 51 citations in OpenAlex.
- Activation of heat shock response to treat obese subjects with type 2 diabetes: a prospective, frequency-escalating, randomized, open-label, triple-arm trial.Scientific reports · 2016Trial
- Heat shock protein 72 (HSP72) modulates glucagon secretion via JNK inhibition in pancreatic α-cells.Diabetology international · 2026Article
- Low-intensity therapeutic ultrasound effects on intracellular sodium and reactive oxygen species in ex vivo human islets for control of insulin release.Ultrasonics · 2025Article
- Combined thermal and mild electrical stimulations modulate heat shock protein and VEGF in retinal pigment epithelial cells under high glucose.BMC research notes · 2025Article
- Pancreatic Antioxidative Defense and Heat Shock Proteins Prevent Islet of Langerhans Cell Death After Chronic Oral Exposure to Cadmium LOAEL Dose.Biological trace element research · 2024Article
- The impact of heat therapy on neuromuscular function and muscle atrophy in diabetic rats.Frontiers in physiology · 2022Article
- NR4A1 enhances MKP7 expression to diminish JNK activation induced by ROS or ER-stress in pancreatic β cells for surviving.Cell death discovery · 2021Article
- Article
- Metabolic control of the proteotoxic stress response: implications in diabetes mellitus and neurodegenerative disorders.Cellular and molecular life sciences : CMLS · 2016Review
- Role of nucleolar protein NOM1 in pancreatic islet β cell apoptosis in diabetes.Experimental and therapeutic medicine · 2016Article
- Effects of heated hydrotherapy on muscle HSP70 and glucose metabolism in old and young vervet monkeys.Cell stress & chaperones · 2016Article
- Effects of heat stress on carbohydrate and lipid metabolism in growing pigs.Physiological reports · 2015Article
- Article
- Induction of Heat Shock Proteins in the Therapy of Type 2 Diabetes and Metabolic Syndrome.EBioMedicine · 2014Article
- Chaperoning to the metabolic party: The emerging therapeutic role of heat-shock proteins in obesity and type 2 diabetes.Molecular metabolism · 2014Review
- The importance of the cellular stress response in the pathogenesis and treatment of type 2 diabetes.Cell stress & chaperones · 2014Article
- The role of heat shock response in insulin resistance and diabetes.Diabetes & metabolism journal · 2014Review
- Article
- Effects of combination therapy with vildagliptin and valsartan in a mouse model of type 2 diabetes.Cardiovascular diabetology · 2013Article
- Mild electrical stimulation at 0.1-ms pulse width induces p53 protein phosphorylation and G2 arrest in human epithelial cells.The Journal of biological chemistry · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Induction of heat shock protein (HSP) 72 improves metabolic profiles in diabetic model mice. However, its effect on pancreatic β-cells is not known. The current study investigated whether HSP72 induction can reduce β-cell stress signaling and apoptosis and preserve β-cell mass. MIN6 cells and db/db mice were sham-treated or treated with heat shock (HS) and mild electrical stimulation (MES) (HS+MES) to induce HSP72. Several cellular markers, metabolic parameters, and β-cell mass were evaluated. HS+MES treatment or HSP72 overexpression increased HSP72 protein levels and decreased tumor necrosis factor (TNF)-α-induced Jun NH(2)-terminal kinase (JNK) phosphorylation, endoplasmic reticulum (ER) stress, and proapoptotic signal in MIN6 cells. In db/db mice, HS+MES treatment for 12 weeks significantly improved insulin sensitivity and glucose homeostasis. Upon glucose challenge, a significant increase in insulin secretion was observed in vivo. Compared with sham treatment, levels of HSP72, insulin, pancreatic duodenal homeobox-1, GLUT2, and insulin receptor substrate-2 were upregulated in the pancreatic islets of HS+MES-treated mice, whereas JNK phosphorylation, nuclear translocation of forkhead box class O-1, and nuclear factor-κB p65 were reduced. Apoptotic signals, ER stress, and oxidative stress markers were attenuated. Thus, HSP72 induction by HS+MES treatment protects β-cells from apoptosis by attenuating JNK activation and cell stresses. HS+MES combination therapy may preserve pancreatic β-cell volume to ameliorate glucose homeostasis in diabetes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.