Dude, hell yea they offer a huge metabolic advantage, especially for those with poor insulin resistance. If insulin is the main “fat storage” hormone, and you keep insulin levels to a minimum, you prime your body to use fat (stored bodyfat, and fats eaten throughout the day) for energy.
As far as your last statement, no offence, it’s completely absurd! Carbs in a traditional diet serves as the main energy source. Without carbs, your body will be forced to swith to fat as long as your protein/fat ratios are correct. Its that simple. By the way, Where did you hear/ retrieve this information from? [/quote]
insulin isn’t the “main fat storage hormone”
when total calorie and protein intakes are matched, ketogenic diets offer NO measurable advantage over non-ketogenic diets.
my last statement isn’t completely absurd. ingested dietary fat can and WILL be stored as bodyfat in the presence of a caloric surplus, even in the total absence of insulin.
J Lipid Res. 1989 Nov;30(11):1727-33. Links
Metabolic response of Acylation Stimulating Protein to an oral fat load.
- Cianflone K,
- Vu H,
- Walsh M,
- Baldo A,
- Sniderman A.
McGill Unit for the Prevention of Cardiovascular Disease, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
Acylation Stimulating Protein (ASP) is a small (mol wt 14,000), basic (pI 9.0) protein present in human plasma. When examined in vitro with normal human cultured skin fibroblasts and adipocytes, ASP appears to be the most potent stimulant of triglyceride synthesis yet described. In this study, a competitive ELISA assay for ASP has been developed using immunospecific polyclonal antibodies, and ASP levels have been measured in seven normal subjects. Following an oral fat load, a sustained significant increase in ASP occurs, whereas after an oral glucose load, ASP levels do not change significantly. These responses are entirely opposite to those of insulin, which rises sharply but transiently after an oral glucose load but is unchanged after an oral fat load. Both the fasting and peak ASP levels were significantly related to the postprandial lipemia. These data provide the first in vivo evidence that Acylation Stimulating Protein may play an important physiological role in the normal response to an oral fat load.
Am J Physiol. 1999 Feb;276(2 Pt 1):E241-8. Links
Effects of an oral and intravenous fat load on adipose tissue and forearm lipid metabolism.
- Evans K,
- Clark ML,
- Frayn KN.
Nuffield Department of Clinical Biochemistry, John Radcliffe Hospital, Headington, Oxford OX3 9DU, UK.
We have studied the fate of lipoprotein lipase (LPL)-derived fatty acids by measuring arteriovenous differences across subcutaneous adipose tissue and skeletal muscle in vivo. Six subjects were fasted overnight and were then given 40 g of triacylglycerol either orally or as an intravenous infusion over 4 h. Intracellular lipolysis (hormone-sensitive lipase action; HSL) was suppressed after both oral and intravenous fat loads (P < 0.001). Insulin, a major regulator of HSL activity, showed little change after either oral or intravenous fat load, suggesting that suppression of HSL action occurred independently of insulin. The rate of action of LPL (measured as triacylglycerol extraction) increased with both oral and intravenous fat loads in adipose tissue (P = 0.002) and skeletal muscle (P = 0.001). There was increased escape of LPL-derived fatty acids into the circulation from adipose tissue, shown by lack of reesterification of fatty acids. There was no release into the circulation of LPL-derived fatty acids from skeletal muscle. These results suggest that insulin is not essential for HSL suppression or increased triacylglycerol clearance but is important in reesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affecting fatty acid partitioning between adipose tissue and the circulation, postprandial nonesterified fatty acid concentrations, and hepatic very low density lipoprotein secretion.
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Int J Obes Relat Metab Disord. 1998 Nov;22(11):1096-102. Links
The influence of oral lipid loads on acylation stimulating protein (ASP) in healthy volunteers.
- Charlesworth JA,
- Peake PW,
- Campbell LV,
- Pussell BA,
- O’Grady S,
- Tzilopoulos T.
Department of Nephrology, Prince Henry Hospital, Little Bay, New South Wales, Australia.
OBJECTIVES: To examine the hypothesis that a sustained rise in plasma acylation stimulating protein (ASP, C3a desarg) accompanies the elevation in triacylglycerol that follows the ingestion of an oral fat load. DESIGN: Following an overnight fast, blood samples were obtained from healthy volunteers while fasting and 15 min, 1, 2, 4, 6 and 8 h following ingestion of: (i) a liquid meal, rich in dairy fat (eight subjects) and (ii) a semi-liquid meal, with higher total fat content and rich in polyunsaturated fat (six subjects). SUBJECTS AND METHODS: Four male and four female volunteers (age range: 22-51 y; body mass index (BMI): 17.9-26.9 kg/m2) received the first meal. Six subjects (age range: 32-60 y; BMI: 18.0-28.4 kg/m2), including three from the first study, received the second meal using the same protocol. ASP and C5a were measured by radioimmunoassay (RIA) and the complement proteins C3, factor B and C5 by radial immunodiffusion or nephelometry. Tumour necrosis factor (TNF)-alpha was measured by enhanced ELISA, and plasma cholesterol and triacylglycerol by an automated enzymatic method. The presence of chylomicrons was assessed in post-prandial plasma samples taken after the second meal. RESULTS: There was no significant change in mean ASP concentration in either group at any time point, following ingestion of either meal. However, there was a significant positive linear trend in ASP following the second fat challenge (ANOVA; P < 0.05). There was also no change in complement proteins, plasma cholesterol or TNF-alpha. Plasma triacylglycerol rose significantly after the first and second meals (P < 0.05 and P < 0.001 at 2 h post-prandially); the mean maximum rise above the fasting level was 58 +/- 41% and 89 +/- 38% respectively (mean +/- s.d.). Chylomicrons were detected in samples taken from each subject after the second meal. Analysis of individual ASP data showed a sustained rise in one subject after the first meal and two subjects after the second meal. Substantial variation in ASP concentration was observed in samples taken in the first 2 h post-prandially. CONCLUSION: There was no significant change in ASP nor other complement proteins for either group of subjects following ingestion of the lipid loads. Individual data showed substantial variation in post-prandial ASP, but multiple plasma sampling did not define the basis for this variation.