The effect of hot-tub therapy on serum Hsp70 level and its benefit on diabetic rats: A preliminary report

Abstract

A decrease in complications in diabetic rats after hot-tub therapy is shown here. An increase in the extracellular Hsp70 level due to HTT was observed. This increase may serve to protect the structure of proteins (e.g. preventing AGE formation), and the observed beneficial effects may be related to it.

The effect of passive heating on heat shock protein 70 and interleukin-6: A possible treatment tool for metabolic diseases?

“…9 The influence of thermal therapy on glycemic regulation and metabolic disease has primarily been investigated using rodent models. 17,18,[25][26][27] . However, there are human data to suggest that local heating at the site of insulin infusion improves postprandial insulin action 28,29 and may benefit long-term glycemic control 29,30 and cardiovascular health in humans.…”

Prior heat stress induces moderation of diabetic alterations in glycogen metabolism of rats

“…These results could be related to the promising effect of sauna therapy for patients with diabetes and other life-style diseases [61], as well as with the helpful hottub therapy for diabetic patients [62] and diabetic rats [63]. Moreover, Kokura et al [7] found that whole body hyperthermia (WBH) may provide a new therapeutic or preventive modality against obesity-related diseases such as type 2 diabetes mellitus and metabolic or insulin resistance syndrome [8].…”

The importance of the cellular stress response in the pathogenesis and treatment of type 2 diabetes

“…Finally, not all studies have found low iHsps in diabetes (Ugurlucan et al 2010). Not infrequently, these studies were in drug-induced, streptozotocin, diabetes, and the acute stress of the sudden diabetic state could raise the levels initially and with time fall to lower levels (Bathaie et al 2010). Low levels of iHsps contribute to an impaired stress response in a disease disrupted by protein glycation and oxidation, free radical formation, protein aggregation, and inflammation, and may be a clue to the etiology of the disease itself for it sets up for disruption of homeostasis and induction of pathology.…”

“…Moreover, diabetics have a decreased amount of slow twitch fibers and correlated to the severity of insulin resistance (Stuart et al 2013). Further debilitating the function of Hsp70 is its glycation, which blocks its protein refolding ability (Bathaie et al 2010). Loss of insulin signaling itself promotes deactivation of HSF1 via an inhibitory phosphorylation of HSF1 by glycogen synthase kinase 3-β (GSK-3β).…”

“…Lastly, heat shock has been shown to protect from loss of organ function (liver, kidney, pancreatic beta cell, and (Kondo et al 2012) Heat and mild electric stimulation: 42°C electrodes and 12 V direct current (55 pps of 0.1 ms duration), 2 times/week for 12-15 weeks Reduced beta cell apoptosis and ER stress, increased insulin response to glucose challenge, reduced cytokine activation Low-dose streptozotocin rat (Bathaie et al 2010) Hot water immersion: rectal temperature 41.0°C for 20 min, 3 times/week, 5 months Lowered fasting glucose, Hb A1c AGE, triglycerides, low-density lipoprotein cholesterol, increased high-density lipoprotein cholesterol, and insulin secretion peripheral nerves). The uniform amelioration of so many of the pathological features associated with t2DM with Hsp induction through nonpharmacologic methods reflects the fundamental role in the initiation and progression of the disease.…”