Insulin resistance in soleus muscle from obese Zucker rats. Involvement of several defective sites
Open accessAbstract
1. The effect of insulin upon glucose transport and metabolism in soleus muscles of genetically obese (fa/fa) and heterozygote lean Zucker rats was investigated at 5–6 weeks and 10–11 weeks of age. Weight-standardized strips of soleus muscles were used rather than the intact muscle in order to circumvent problems of diffusion of substrates. 2. In younger obese rats (5–6 weeks), plasma concentrations of immunoreactive insulin were twice those of controls, whereas their circulating triacylglycerol concentrations were normal. Insulin effects upon 2-deoxyglucose uptake and glucose metabolism by soleus muscles of these rats were characterized by both a decreased sensitivity and a decrease in the maximal response of this tissue to the hormone. 3. In older obese rats (10–11 weeks), circulating concentrations of insulin and triacylglycerols were both abnormally elevated. A decrease of 25–35% in insulin-binding capacity to muscles of obese rats was observed. The soleus muscles from the older obese animals also displayed decreased sensitivity and maximal response to insulin. However, at a low insulin concentration (0.1m-i.u./ml), 2-deoxyglucose uptake by muscles of older obese rats was stimulated, but such a concentration was ineffective in stimulating glucose incorporation into glycogen, and glucose metabolism by glycolysis. 4. Endogenous lipid utilization by muscle was calculated from the measurements of O2 consumption, and glucose oxidation to CO2. The rate of utilization of fatty acids was normal in muscles of younger obese animals, but increased in those of the older obese rats. Increased basal concentrations of citrate, glucose 6-phosphate and glycogen were found in muscles of older obese rats and may reflect intracellular inhibition of glucose metabolism as a result of increased lipid utilization. 5. Thus several abnormalities are responsible for insulin resistance of muscles from obese Zucker rats among which we have observed decreased insulin binding, decreased glucose transport and increased utilization of endogenous fatty acid which could inhibit glucose utilization.
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In some animal models of obesity, skeletal muscle shows a metabolic profile characterized by reduced glucose uptake and glucose oxidation, altered partitioning of fatty acids that are incorporated into triglycerides, and reduced oxygen consumption.
“In some animal models of obesity such as in obese Zucker rats or ob/ob mice, skeletal muscle shows a metabolic profile characterized by reduced glucose uptake and glucose oxidation, altered partitioning of fatty acids that are incorporated into triglycerides, and reduced oxygen consumption (14 -18).”
From Expression of <i>Mfn2</i>, the Charcot-Marie-Tooth Neuropathy Type 2A Gene, in Human Skeletal Muscle (2005) · cites this paper as [16]
The sections on glucose uptake and intracellular metabolism report impaired glucose uptake and reduced glucose oxidation in older obese Zucker rats. They also report higher muscle triacylglycerol content and increased fatty-acid utilization, but not fatty-acid incorporation into triglycerides. Contrary to the oxygen-consumption part of the claim, the Defects in intracellular metabolism section says oxygen consumption was unchanged versus controls; the study does not examine ob/ob mice. Page numbers were not available in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredIn some animal models of obesity such as obese Zucker rats or ob/ob mice, skeletal muscle shows a metabolic profile characterized by reduced glucose uptake and glucose oxidation, altered partitioning of fatty acids, insulin resistance and reduced oxygen consumption.
“In some animal models of obesity such as in obese Zucker rats or ob/ob mice, skeletal muscle shows a metabolic profile characterized by reduced glucose uptake and glucose oxidation, altered partitioning of fatty acids that are incorporated into triglycerides, or oxidized, insulin resistance and reduced oxygen consumption (38-43”
From Mitofusin-2 Determines Mitochondrial Network Architecture and Mitochondrial Metabolism (2003) · cites this paper as [40]
The paper’s opening summary reports reduced insulin-stimulated glucose uptake and insulin resistance in obese Zucker rat soleus muscle; the ‘Defects in intracellular metabolism’ section reports reduced glucose oxidation and greater lipid utilization in older obese rats. That section also says oxygen consumption was unchanged compared with controls, contrary to the claimed reduction. The paper does not establish this entire profile for ob/ob mice or measure fatty-acid incorporation into triglycerides. (LLM, conf=0.90)
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References 31 · Cited by 311
Research works printed but not linked: 6
- Bergmeyer, H. U. & Bernt, E. (1974b) in Methods of Enzymatic Analysis (Bergmeyer, H. U., ed.), 2nd English edn., pp. 1205-1215, Academic Press, New York and London
- Bray, G. A. (1977) Fed. Proc. Fed. Am. Soc. Exp. Biol. 36, 148-153
- Jaworek, D., Gruber, W. & Bergmeyer, H. U. (1974) in Methods of Enzymatic Analysis (Bergmeyer, H. U., ed.), 2nd English edn., pp. 2127-2131. Academic Press, New York and London
- Lamprecht, W., Stein, P., Heinz, F. & Weisser, H. (1974) in Methods of Enzymatic Analysis (Bergmeyer, H. U., ed.), 2nd English edn., pp. 1777-1779, Academic Press, New York and London
- Lang, G. & Gerhard, M. (1974) Methods of Enzymatic Analysis (Bergmeyer, H. U., ed.), 2nd English edn., pp. 1238-1242, Academic Press, New York and London
- Passonneau, J. V. & Brown, J. G. (1974) in Methods of Enzymatic Analysis (Bergmeyer, H. U., ed.), 2nd Eng- lish edn., pp. 1565-1569, Academic Press, New York and London
- Authors
- Crettaz, M., Prentki, M., Zaninetti, D., & Jeanrenaud, B.
- Affiliations
- University of Geneva (CH)
- ORCID
- Prentki, Marc
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 1980-02-15
- Volume
- 186
- Issue
- 2
- Pages
- 525-534
- ISSN
- 0306-3283 (ISSN-L)
- PMC
- PMC1161605
- OpenAlex
- W28452575
- Cited by
- 311
- References
- 31
- Citations by year
- 2024: 1 · 2023: 1 · 2022: 3 · 2018: 1 · 2017: 6 · 2016: 4 · 2015: 3 · 2014: 6 · 2013: 3 · 2012: 8
- FWCI
- 4.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biochemical Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- insulin resistance, soleus muscle, Zucker fatty rats, obesity, insulin binding, glucose transport, 2-deoxyglucose uptake, glucose metabolism, fatty acid utilization, lipid utilization, glycogen, triglycerides, insulin sensitivity, age-related changes
- MeSH terms
- Animals, Deoxyglucose, Female, Glucose, Glycogen, Glycolysis, Insulin, Insulin Resistance, Intracellular Fluid, Muscles, Obesity, Oxygen Consumption, Receptor, Insulin, Rats, In Vitro Techniques
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