Difference between revisions of "Gupte 2009 Diabetes"
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{{Publication | {{Publication | ||
|title=Gupte AA, Bomhoff GL, Swerdlow RH, Geiger PC (2009) Heat treatment improves glucose tolerance and prevents skeletal muscle insulin resistance in rats fed a high-fat diet. Diabetes | |title=Gupte AA, Bomhoff GL, Swerdlow RH, Geiger PC (2009) Heat treatment improves glucose tolerance and prevents skeletal muscle insulin resistance in rats fed a high-fat diet. Diabetes 58:567-78. | ||
|authors=Gupte AA, Bomhoff GL, Swerdlow RH, Geiger PC Ā | |info=[http://www.ncbi.nlm.nih.gov/pubmed/19073766 PMID: 19073766 Open Access] | ||
|authors=Gupte AA, Bomhoff GL, Swerdlow RH, Geiger PC | |||
|year=2009 | |year=2009 | ||
|journal=Diabetes | |journal=Diabetes | ||
|abstract=OBJECTIVEāHeat treatment and overexpression of heat | |abstract=OBJECTIVEāHeat treatment and overexpression of heat shock protein 72 (HSP72) have been shown to protect against high-fat dietāinduced insulin resistance, but little is known about the underlying mechanism or the target tissue of HSP action. The purpose of this study is to determine whether ''in vivo'' heat treatment can prevent skeletal muscle insulin resistance. | ||
shock protein 72 (HSP72) have been shown to protect against | RESEARCH DESIGN AND METHODSāMale Wistar rats were fed a high-fat diet (60% calories from fat) for 12 weeks and received a lower-body heat treatment (41Ā°C for 20 min) once per week. | ||
high-fat dietāinduced insulin resistance, but little is known about | Ā | ||
the underlying mechanism or the target tissue of HSP action. The | RESULTSāOur results show that heat treatment shifts the metabolic characteristics of rats on a high-fat diet toward those on a standard diet. Heat treatment improved glucose tolerance, restored insulin-stimulated glucose transport, and increased insulin signaling in soleus and extensor digitorum longus (EDL) muscles from rats fed a high-fat diet. Heat treatment resulted in decreased activation of Jun NH2-terminal kinase (JNK) and inhibitor of kB kinase (IKK-Ī²), stress kinases implicated in insulin resistance, and upregulation of HSP72 and HSP25, proteins previously shown to inhibit JNK and IKK-Ī² activation, respectively. Mitochondrial citrate synthase and cytochrome oxidase activity decreased slightly with the high-fat diet, but heat treatment restored these activities. Data from L6 cells suggest that one bout of heat treatment increases mitochondrial oxygen consumption and fatty acid oxidation. | ||
purpose of this study is to determine whether in vivo heat | Ā | ||
treatment can prevent skeletal muscle insulin resistance. | CONCLUSIONSāOur results indicate that heat treatment protects skeletal muscle from high-fat dietāinduced insulin resistance and provide strong evidence that HSP induction in skeletal muscle could be a potential therapeutic treatment for obesity induced insulin resistance [http://healthy-ojas.com/diabetes/diabetes-details.html diabetes]. | ||
RESEARCH DESIGN AND METHODSāMale Wistar rats | |keywords=Heat shock protein 72 (HSP72), Insulin, High-fat diet, Mitochondria | ||
were fed a high-fat diet (60% calories from fat) for 12 weeks and | |mipnetlab=US KS Kansas City Swerdlow RH | ||
received a lower-body heat treatment (41Ā°C for 20 min) once per | |discipline=Biomedicine, Pharmacology; Biotechnology | ||
week. | |||
RESULTSāOur results show that heat treatment shifts the | |||
metabolic characteristics of rats on a high-fat diet toward those | |||
on a standard diet. Heat treatment improved glucose tolerance, | |||
restored insulin-stimulated glucose transport, and increased insulin | |||
signaling in soleus and extensor digitorum longus (EDL) | |||
muscles from rats fed a high-fat diet. Heat treatment resulted in | |||
decreased activation of Jun NH2-terminal kinase (JNK) and | |||
inhibitor of | |||
insulin resistance, and upregulation of HSP72 and HSP25, proteins | |||
previously shown to inhibit JNK and IKK- | |||
respectively. Mitochondrial citrate synthase and cytochrome | |||
oxidase activity decreased slightly with the high-fat diet, but heat | |||
treatment restored these activities. Data from L6 cells suggest | |||
that one bout of heat treatment increases mitochondrial oxygen | |||
consumption and fatty acid oxidation. | |||
CONCLUSIONSāOur results indicate that heat treatment protects | |||
skeletal muscle from high-fat dietāinduced insulin resistance | |||
and provide strong evidence that HSP induction in skeletal | |||
muscle could be a potential therapeutic treatment for | |||
insulin resistance | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, Exercise physiology;nutrition;life style | |||
|organism=Rat | |||
|tissues=Skeletal muscle | |||
|enzymes=Complex III, Complex IV;cytochrome c oxidase | |||
|diseases=Diabetes | |||
|topics=ADP, Substrate, Temperature, Fatty acid | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
| | |discipline=Biomedicine, Pharmacology; Biotechnology | ||
}} | }} | ||
Latest revision as of 10:58, 3 December 2019
| Gupte AA, Bomhoff GL, Swerdlow RH, Geiger PC (2009) Heat treatment improves glucose tolerance and prevents skeletal muscle insulin resistance in rats fed a high-fat diet. Diabetes 58:567-78. |
Gupte AA, Bomhoff GL, Swerdlow RH, Geiger PC (2009) Diabetes
Abstract: OBJECTIVEāHeat treatment and overexpression of heat shock protein 72 (HSP72) have been shown to protect against high-fat dietāinduced insulin resistance, but little is known about the underlying mechanism or the target tissue of HSP action. The purpose of this study is to determine whether in vivo heat treatment can prevent skeletal muscle insulin resistance. RESEARCH DESIGN AND METHODSāMale Wistar rats were fed a high-fat diet (60% calories from fat) for 12 weeks and received a lower-body heat treatment (41Ā°C for 20 min) once per week.
RESULTSāOur results show that heat treatment shifts the metabolic characteristics of rats on a high-fat diet toward those on a standard diet. Heat treatment improved glucose tolerance, restored insulin-stimulated glucose transport, and increased insulin signaling in soleus and extensor digitorum longus (EDL) muscles from rats fed a high-fat diet. Heat treatment resulted in decreased activation of Jun NH2-terminal kinase (JNK) and inhibitor of kB kinase (IKK-Ī²), stress kinases implicated in insulin resistance, and upregulation of HSP72 and HSP25, proteins previously shown to inhibit JNK and IKK-Ī² activation, respectively. Mitochondrial citrate synthase and cytochrome oxidase activity decreased slightly with the high-fat diet, but heat treatment restored these activities. Data from L6 cells suggest that one bout of heat treatment increases mitochondrial oxygen consumption and fatty acid oxidation.
CONCLUSIONSāOur results indicate that heat treatment protects skeletal muscle from high-fat dietāinduced insulin resistance and provide strong evidence that HSP induction in skeletal muscle could be a potential therapeutic treatment for obesity induced insulin resistance diabetes. ā¢ Keywords: Heat shock protein 72 (HSP72), Insulin, High-fat diet, Mitochondria
ā¢ O2k-Network Lab: US KS Kansas City Swerdlow RH
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Pathology: Diabetes
Organism: Rat Tissue;cell: Skeletal muscle
Enzyme: Complex III, Complex IV;cytochrome c oxidase Regulation: ADP, Substrate, Temperature, Fatty acid Coupling state: OXPHOS
HRR: Oxygraph-2k
