Wed, Mar-24-04, 21:20
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Experimenter
Posts: 25,940
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Plan: DDF
Stats: 202/185.4/179
BF:
Progress: 72%
Location: San Diego, CA
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Ok, here's some studies I found at: http://www.ncbi.nlm.nih.gov, I did a search on "insulin aspartame"
Presumably all peer-reviewed and published in respected scientific and research journals, not from random nutritionists promoting a book or with an agenda.
Now, I'm not a metabolic scientist, so I have to struggle to understand these. The first one seems to indicate that the phenylalanine in aspartame gives you a feeling of saiety and theyr'e trying to figure out how. phenylalanine was commonly used in OTC diet pills for a long time, maybe still is. I know it is a supplement you could also buy at a Health food store. Anyway, interesting but the real reason I included it was because it shows no rise in glucose or insulin when you consume it.
Quote:
Physiological mechanisms mediating aspartame-induced satiety.
Hall WL, Millward DJ, Rogers PJ, Morgan LM.
Centre for Nutrition and Food Safety, School of Biomedical and Life Sciences, University of Surrey, Guildford, Surrey GU2 7XH, UK. w.l.hall~reading.ac.uk
Aspartame has been previously shown to increase satiety. This study aimed to investigate a possible role for the satiety hormones cholecystokinin (CCK) and glucagon-like peptide-1 (GLP-1) in this effect. The effects of the constituents of aspartame, phenylalanine and aspartic acid, were also examined. Six subjects consumed an encapsulated preload consisting of either 400 mg aspartame, 176 mg aspartic acid+224 mg phenylalanine, or 400 mg corn flour (control), with 1.5 g paracetamol dissolved in 450 ml water to measure gastric emptying. A 1983-kJ liquid meal was consumed 60 min later. Plasma CCK, GLP-1, glucose-dependent insulinotropic polypeptide (GIP), glucose, and insulin were measured over 0-120 min. Gastric emptying was measured from 0 to 60 min. Plasma GLP-1 concentrations decreased following the liquid meal (60-120 min) after both the aspartame and amino acids preloads (control, 2096.9 pmol/l min; aspartame, 536.6 pmol/l min; amino acids, 861.8 pmol/l min; incremental area under the curve [AUC] 60-120 min, P<.05). Desire to eat was reduced from 60 to 120 min following the amino acids preload (control, -337.1 mm min; aspartame, -505.4 mm min; amino acids, -1497.1 mm min; incremental AUC 60-120 min, P<.05). However, gastric emptying rates, plasma CCK, GIP, insulin, and glucose concentrations were unaffected. There was a correlation between the increase in plasma phenylalanine and decrease in desire to eat after the liquid meal following the constituent amino acids (r=-.9774, P=.004). In conclusion, it is unlikely that aspartame increases satiety via CCK- or GLP-1-mediated mechanisms, but small changes in circulating phenylalanine concentrations may influence appetite.
Publication Types:
Clinical Trial
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This one showed that mice ingesting ASP lost weight compared to ones on regular old water.
Quote:
Effects of long-term ingestion of aspartame on hypothalamic neuropeptide Y, plasma leptin and body weight gain and composition.
Beck B, Burlet A, Max JP, Stricker-Krongrad A.
Centre de Recherches UHP/EA 3453, IFR no. 111, Systemes Neuromodulateurs des Comportements Ingestifs; 38, rue Lionnois, 54000 Nancy, France. bernard.beck~nancy.inserm.fr
The aim of this study was to determine the effects of the chronic ingestion of aspartame (ASP) on brain neuropeptide Y (NPY) concentrations, plasma hormones, food intake and body fat. Two groups of male Long-Evans rats, fed on a control (C) well-balanced diet, had to drink either a 0.1% ASP solution or water for a period of 14 weeks starting at weaning. Food intake and body weight were weekly recorded. At the end of the experiment, fat pads were sampled, leptin and insulin were measured in the plasma and NPY in several microdissected brain areas. Substituting ASP for water led to lower body weight (-8%; P<.004) and lower fat depot weight (-20%; P<.01) with no differences in energy intake or plasma insulin concentrations. Plasma leptin was significantly reduced by 34% (P<.05). Leptin concentrations were well-correlated with final body weight (r=.47; P<.025) and fat pad mass (r=.53; P<.01). NPY concentrations were 23% lower (P<.03) in the arcuate nucleus of ASP rats with no differences in other brain areas. The beneficial effects on body composition could be related to the decreased effects of NPY on lipid and energy metabolism, independently of insulin. The reasons for the NPY decrease (regulatory or toxicological) are not obvious. The constitutive amino acids of the ASP molecule might participate in the NPY regulation.
PMID: 11890951 [PubMed - indexed for MEDLINE]
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And then this one is interesting! It shows that bitter tastes might actually cause the pancreas to release insulin. However, aspartame has no bitter taste to it. However, some sweeteners do!
Quote:
Effects of artificial sweeteners on insulin release and cationic fluxes in rat pancreatic islets.
Malaisse WJ, Vanonderbergen A, Louchami K, Jijakli H, Malaisse-Lagae F.
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
Beta-L-glucose pentaacetate, but not alpha-D-galactose pentaacetate, was recently reported to taste bitter and to stimulate insulin release. This finding led, in the present study, to the investigation of the effects of both bitter and non-bitter artificial sweeteners on insulin release and cationic fluxes in isolated rat pancreatic islets. Sodium saccharin (1.0-10.0 mM), sodium cyclamate (5.0-10.0 mM), stevioside (1.0 mM) and acesulfame-K (1.0-15.0 mM), all of which display a bitter taste, augmented insulin release from islets incubated in the presence of 7.0 mM D-glucose. In contrast, aspartame (1.0-10.0 mM), which is devoid of bitter taste, failed to affect insulin secretion. A positive secretory response to acesulfame-K was still observed when the extracellular K+ concentration was adjusted to the same value as that in control media. No major changes in 86Rb and 45Ca outflow from pre-labelled perifused islets could be attributed to the saccharin, cyclamic or acesulfame anions. It is proposed that the insulinotropic action of some artificial sweeteners and, possibly, that of selected hexose pentaacetate esters may require G-protein-coupled receptors similar to those operative in the recognition of bitter compounds by taste buds.
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And here's another one specifically testing artificial sweeteners and insulin release.
Quote:
Sweet taste: effect on cephalic phase insulin release in men.
Teff KL, Devine J, Engelman K.
Monell Chemical Senses Center, Philadelphia, PA 19104, USA.
To determine whether sweet-tasting solutions are effective elicitors of cephalic phase insulin release (CPIR) in humans, two studies were conducted using nutritive and nonnutritive sweeteners as stimuli. Normal weight men sipped and spit four different solutions: water, aspartame, saccharin, and sucrose. A fifth condition involved a modified sham-feed with apple pie. The five stimuli were administered in counterbalanced order, each on a separate day. In study 1, subjects tasted the stimuli for 1 min (n = 15) and in study 2 (n = 16), they tasted the stimuli for 3 min. Arterialized venous blood was drawn to establish a baseline and then at 1 min poststimulus, followed by every 2 min for 15 min and then every 5 min for 15 min. In both study 1 and study 2, no significant increases in plasma insulin were observed after subjects tasted the sweetened solutions. In contrast, significant increases in plasma insulin occurred after the modified sham-feed with both the 1 min and 3 min exposure. These results suggest that nutritive and nonnutritive sweeteners in solution are not adequate stimuli for the elicitation of CPIR.
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