Fatty acid oxidation and control of food intake

Leonhardt, M.; Langhans, Wolfgang

doi:10.1016/j.physbeh.2004.07.033

Cited by 83 publications

(64 citation statements)

References 60 publications

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“…Furthermore, the n-3 polyunsaturated fatty acids promote the expression of genes encoding proteins involved in fatty acid oxidation. An increased oxidation of fat also promotes satiety for fat, 12 which aids in preventing weight gain with a fat diet enriched in n-3 polyunsaturated fatty acids. Thus, in order for the lowcarbohydrate/high-fat diet to be health promoting, the type of fat is important and must include polyunsaturated fatty acids.…”

Section: The Composition Of the Dietary Fat Is Important For Satiety mentioning

confidence: 99%

The effect of low carbohydrate on energy metabolism

Erlanson–Albertsson

Mei

2005

Int J Obes

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OBJECTIVE: To investigate whether low-carbohydrate diets are efficient for reduction of body weight and through which mechanism. DESIGN: A couple of studies using low-carbohydrate diets in the treatment of obesity are reviewed. Mechanisms for explaining the reduced appetite are described in relation to knowledge on regulation of appetite for fat and carbohydrate. RESULTS: Studies with low-carbohydrate diets demonstrate a rapid weight loss, being more pronounced after 3 and 6 months compared to low-fat diets. After 12 months there is no difference between the low-carbohydrate and the conventional low-fat diet on weight loss. Both diets lead to improvements in risk factors for coronary heart disease, the low-carbohydrate diet leading to a greater decrease in serum triglycerides and increase in HDL cholesterol compared to the low-fat diet. Blood pressure, insulin sensitivity and LDL cholesterol were improved to a similar degree by the two diets. The mechanism for the rapid weight loss with the low-carbohydrate diet is a suppressed appetite, first through the high-protein content of the diet, second through the ketogenic nature of the diet with satiety signals for fat being active and third through the absence of hunger-promoting carbohydrate components like sucrose and/or fructose. CONCLUSION: A rapid initial weight loss occurs with a low-carbohydrate diet due to a suppressed appetite. There is as yet no indication of an increased metabolic rate and an increased thermogenesis by the low-carbohydrate diet. The safety and efficacy of low-carbohydrate diets have to await further studies.

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Section: The Composition Of the Dietary Fat Is Important For Satiety mentioning

confidence: 99%

The effect of low carbohydrate on energy metabolism

Erlanson–Albertsson

Mei

2005

Int J Obes

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“…Extensive evidence indicates that hepatic FAO can control food intake [11,15,18]. This study was designed to test the hypothesis that, due to the more rapid hepatic oxidation of MCFA than LCFA, HPV infusion of the MCFA CAwould inhibit feeding more potently than HPV infusion of comparable amounts of the LCFA OA.…”

Section: Discussionmentioning

confidence: 99%

“…Vagal afferent signaling apparently mediates much of the control of food intake by lipids in the small intestine [6,7,35] as well as by hepatic lipid metabolism [18]. Vagal receptors with different sensitivity to LCFA and MCFA have been identified in the small intestine [19], and HPV infusion of the LCFA linoleic acid increased hepatic vagal afferent activity more than the same amount of CA [28].…”

Section: Discussionmentioning

confidence: 99%

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Hepatic-portal oleic acid inhibits feeding more potently than hepatic-portal caprylic acid in rats

Sousa

Benthem

Arsenijevic

et al. 2006

Physiology & Behavior

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. Hepatic-portal oleic acid inhibits feeding more potently than hepatic-portal caprylic acid in rats. Physiology and Behavior, 89(3), 329-334. https://doi.org/10.1016/j.physbeh.2006.06.020 Copyright Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. AbstractIn several human and animal studies, medium-chain triglycerides decreased food intake more than did long-chain triglycerides. It is possible that faster uptake and metabolism of medium-chain fatty acids in the liver is responsible for this difference. To test this hypothesis we compared the feeding effects of hepatic portal vein (HPV) infusion of the medium-chain fatty acid caprylic acid (CA) with those of the long-chain fatty acid oleic acid (OA). Contrary to our expectation, six-h HPV infusion of 14 μg/min (50 nmol/min) OA robustly inhibited feeding, whereas infusion of 22 or 220 μg/min (150 and 1500 nmol/min) CA failed to have any effect on feeding. Only a much larger dose of CA, 1100 μg/min (7500 nmol/ min) inhibited feeding similarly to 14 μg/min OA. The increased feeding-inhibitory potency of OA did not appear to be due to differences in stimulation of hepatic fatty acid oxidation because equimolar (50 nmol/min) doses of OA (14 μg/min) and CA (7 μg/min) did not differentially affect post-infusion levels of β-hydroxybutyrate. Stress, inflammation, acute hepatotoxicity or oxidative stress also do not appear to account for the increased feeding-inhibitory potency of HPV OA because plasma concentrations of the stress hormones corticosterone and epinephrine, the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-α, the liver enzymes γ-glutamyl transferase and alanine aminotransferase and as well as hepatic levels of malondialdehyde and glutathione were all similar after HPV infusion of saline or of 50 nmol/min OA or CA.

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“…Efficient hepatic fatty acid oxidation sends a satiety signal to the brain via the vagus nerve; this mechanism likely contributes to the satiety associated with prolonged fasting (Scharrer 1999;Leonhardt and Langhans 2004;St-Onge and Jones 2002). Moreover, it is intriguing to note that expression of a constitutively active form of AMPKα2 in mouse liver induces uncoupling protein-2 (UCP-2)-possibly owing to increased function of Foxo3a and PGC-1alpha, which drive its transcription in endothelial cells (Olmos et al 2009;Foretz et al 2005;Xie et al 2008).…”

Section: Weight Controlmentioning

confidence: 99%

AMPK activation—protean potential for boosting healthspan

McCarty

2013

AGE

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AMP-activated kinase (AMPK) is activated when the cellular (AMP+ADP)/ATP ratio rises; it therefore serves as a detector of cellular "fuel deficiency." AMPK activation is suspected to mediate some of the health-protective effects of long-term calorie restriction. Several drugs and nutraceuticals which slightly and safely impede the efficiency of mitochondrial ATP g e n e r a t i o n -m o s t n o t a b l y m e t f o r m i n a n d berberine-can be employed as clinical AMPK activators and, hence, may have potential as calorie restriction mimetics for extending healthspan. Indeed, current evidence indicates that AMPK activators may reduce risk for atherosclerosis, heart attack, and stroke; help to prevent ventricular hypertrophy and manage congestive failure; ameliorate metabolic syndrome, reduce risk for type 2 diabetes, and aid glycemic control in diabetics; reduce risk for weight gain; decrease risk for a number of common cancers while improving prognosis in cancer therapy; decrease risk for dementia and possibly other neurodegenerative disorders; help to preserve the proper structure of bone and cartilage; and possibly aid in the prevention and control of autoimmunity. While metformin and berberine appear to have the greatest utility as clinical AMPK activators-as reflected by their efficacy in diabetes management-regular ingestion of vinegar, as well as moderate alcohol consumption, may also achieve a modest degree of healthprotective AMPK activation. The activation of AMPK achievable with any of these measures may be potentiated by clinical doses of the drug salicylate, which can bind to AMPK and activate it allosterically.

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Fatty acid oxidation and control of food intake

Cited by 83 publications

References 60 publications

The effect of low carbohydrate on energy metabolism

The effect of low carbohydrate on energy metabolism

Hepatic-portal oleic acid inhibits feeding more potently than hepatic-portal caprylic acid in rats

AMPK activation—protean potential for boosting healthspan

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