Feeding, fasting and starvation: factors affecting fuel utilization

Macdonald, I. A.; Webber, Jonathan

doi:10.1079/pns19950053

Cited by 29 publications

(22 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is generally accepted that FFAs derived from adipose lipolysis are the only important source for lipid oxidation during caloric restriction (12,28). On the other hand, these ideas about FFAs were conceived before the recent discovery of lipolysis in skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Evidence for a Major Role of Skeletal Muscle Lipolysis in the Regulation of Lipid Oxidation During Caloric Restriction In Vivo

Hagström-Toft¹,

Thörne

Reynisdottir³

et al. 2001

Diabetes

View full text Add to dashboard Cite

A lipolytic process in skeletal muscle has recently been demonstrated. However, the physiological importance of this process is unknown. We investigated the role of skeletal muscle lipolysis for lipid utilization during caloric restriction in eight obese women before and after 11 days of very low-calorie diet (VLCD) (2.2 MJ per day). Subjects were studied with indirect calorimetry and microdialysis of skeletal muscle and adipose tissue in order to analyze substrate utilization and glycerol (lipolysis index) in connection with a two-step euglycemic-hyperinsulinemic (12 and 80 mU/m 2 ⅐ min) clamp. Local blood flow rates in the two tissues were determined with 133 Xe-clearance. Circulating free fatty acids and glycerol decreased to a similar extent during insulin infusion before and during VLCD, and there was a less marked insulin-induced reduction in lipid oxidation during VLCD. Adipose tissue glycerol release was hampered by insulin infusion to the same extent (ϳ40%) before and during VLCD. Skeletal muscle glycerol release was not influenced by insulin before VLCD. However, during VLCD insulin caused a marked (fivefold) (P < 0.01) increase in skeletal muscle glycerol release. The effect was accompanied by a fourfold stimulation of skeletal muscle blood flow (P < 0.01). We propose that, during short-term caloric restriction, the reduced ability of insulin to inhibit lipids, despite a preserved antilipolytic effect of the hormone in adipose tissue, is caused by an augmented mobilization of fat from skeletal muscle, and that a physiological role of muscle lipolysis provides a local source of fatty acids.

show abstract

Section: Discussionmentioning

confidence: 99%

“…The FFAs liberated are subsequently used for lipid oxidation, which mainly occurs in skeletal muscle. However, it has been generally accepted that FFAs derive from lipolysis in adipose tissue during caloric restriction (12).…”

mentioning

confidence: 99%

Evidence for a Major Role of Skeletal Muscle Lipolysis in the Regulation of Lipid Oxidation During Caloric Restriction In Vivo

Hagström-Toft¹,

Thörne

Reynisdottir³

et al. 2001

Diabetes

View full text Add to dashboard Cite

show abstract

“…Data (a-j) are means ± SD; *p<0.05, **p<0.005 and ***p<0.001 compared with LPS only-treated groups balance could affect fat mass and adipocyte size [45]. A reduction of food intake in animals is usually accompanied by a reduction of energy use [46]. However, we did not observe any differences in energy expenditure in rAd-GLP-1-treated mice compared with rAd-βgal-treated mice, despite a significant decrease in food intake in the former.…”

Section: Discussionmentioning

confidence: 99%

Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes

et al. 2012

View full text Add to dashboard Cite

Aims/hypothesis Obesity and insulin resistance are associated with low-grade chronic inflammation. Glucagon-like peptide-1 (GLP-1) is known to reduce insulin resistance. We investigated whether GLP-1 has anti-inflammatory effects on adipose tissue, including adipocytes and adipose tissue macrophages (ATM). Methods We administered a recombinant adenovirus (rAd) producing GLP-1 (rAd-GLP-1) to an ob/ob mouse model of diabetes. We examined insulin sensitivity, body fat mass, the infiltration of ATM and metabolic profiles. We analysed the mRNA expression of inflammatory cytokines, lipogenic genes, and M1 and M2 macrophage-specific genes in adipose tissue by real-time quantitative PCR. We also examined the activation of nuclear factor κB (NF-κB), extracellular signalregulated kinase 1/2 and Jun N-terminal kinase (JNK) in vivo and in vitro. Results Fat mass, adipocyte size and mRNA expression of lipogenic genes were significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Macrophage populations (F4/80 + and F4/80 + CD11b + CD11c + cells), as well as the expression and production of IL-6, TNF-α and monocyte chemoattractant protein-1, were significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Expression of M1-specific mRNAs was significantly reduced, but that of M2-specific mRNAs was unchanged in rAd-GLP-1-treated ob/ob mice. NF-κB and JNK activation was significantly reduced in adipose tissue of rAd-GLP-1-treated ob/ob mice. Lipopolysaccharide-induced inflammation was reduced by the GLP-1 receptor agonist, exendin-4, in 3T3-L1 adipocytes and ATM. Conclusions/interpretation We suggest that GLP-1 reduces macrophage infiltration and directly inhibits inflammatory pathways in adipocytes and ATM, possibly contributing to the improvement of insulin sensitivity.

show abstract

“…The metabolic changes that occur during fasting have been well characterized [28]. Initially, hepatic reserves of glycogen are broken down by glycogenolysis, liberating glucose, which is exported into the circulation.…”

Section: The Role Of Ketone Bodies During Fastingmentioning

confidence: 99%

The biochemistry of ketogenesis and its role in weight management, neurological disease and oxidative stress

McPherson

McEneny

2011

J Physiol Biochem

View full text Add to dashboard Cite

Ketogenesis is the branch of mammalian metabolism concerned with the synthesis of ketone bodies. In this process, the small, water-soluble compounds acetoacetate, D-3-β-hydroxybutyrate and propanone are produced by the liver in response to reduced glucose availability. Although ketone bodies are always present at a low level in healthy individuals, dietary manipulation and certain pathological conditions can increase the levels of these compounds in vivo. In some instances, such as in refractory epilepsy, high levels of ketone bodies can be beneficial-in this instance, by exerting an anticonvulsant effect. Conversely, if the levels of ketones rise to supraphysiological levels, as can occur in diabetes mellitus, a state of ketoacidosis can occur, which has serious consequences for cellular function. More recently, research has identified a possible link between ketogenesis and free radical-mediated pathologies, highlighting the potential application of ketogenic diets to the treatment of conditions such as Alzheimer's disease. Overall, an understanding of ketone body metabolism and its links to human disease may prove to be vital in developing new regimens for the treatment of human disease.

show abstract

Feeding, fasting and starvation: factors affecting fuel utilization

Cited by 29 publications

References 24 publications

Evidence for a Major Role of Skeletal Muscle Lipolysis in the Regulation of Lipid Oxidation During Caloric Restriction In Vivo

Evidence for a Major Role of Skeletal Muscle Lipolysis in the Regulation of Lipid Oxidation During Caloric Restriction In Vivo

Glucagon-like peptide-1 inhibits adipose tissue macrophage infiltration and inflammation in an obese mouse model of diabetes

The biochemistry of ketogenesis and its role in weight management, neurological disease and oxidative stress

Contact Info

Product

Resources

About