Bingo! Thanks Miles and Michael. Just what I was looking for.
Here's some fascinating stuff I found on lingual lipase:
Lingual Lipasehttp://en.wikipedia.org/wiki/Lingual_lipase“In the uterus, the fetus is dependent on a high-carbohydrate diet. After birth, fat in milk or a milk substitute becomes the major source of nutrition. Absorptive rates of dietary fat are much lower in neonates than in adults, 65-80% as compared to >95% respectively, which can be attributed to low pancreatic lipase activity. (1 Hamosh M, Scow RO (January 1973). "Lingual lipase and its role in the digestion of dietary lipid". J. Clin. Invest. 52 (1): 88 – 95. doi:10.1172/JCI107177. PMID 4682389) Furthermore, milk fat is not a good substrate for pancreatic lipase. This fact, in combination with the bile salt deficiency and low pH throughout the gastrointestinal tract of the neonate, demands that lingual lipase be the main enzyme catalyzing the hydrolysis of dietary fat. This enzyme activity has been seen as early as 26 weeks gestational age, with ability to hydrolyze dietary fats variable according to digestive tract maturity.(1)”
Human distribution of lingual lipase within the body is more like that of other primates and carnivores than of plant-heavy omnivores and ruminants:
From Fat digestion and absorption, By Armand B. Christophe, Stephanie DeVriese, p. 1:
“(L)ingual lipase is present in rodents and ruminants who have no gastric lipase, whereas carnivores, lagomorphs, and primates, including humans, have predominantly gastric lipase.”
Oral lingual lipase continues to work in the stomach of rats:
Lingual Lipase and Its Role in the Digestion of Dietary Lipidhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC302230/?tool=pmcentrez(emphasis mine)
Abstract
“The serous glands of rat tongue were found to contain a potent lipolytic enzyme which hydrolyzed triglyceride to mostly
diglyceride and free fatty acids (FFA) at pH 4.5-5.4. Homogenates of lingual serous glands from adult rats hydrolyzed 40-70 mmol of triglyceride/g per h. The soft palate, anterior oral pharyngeal wall, and lateral oral pharyngeal glands also contained the activity, but at a much lower level. The lipolytic activity was also found in saliva collected through an esophageal cannula and in stomach contents of rats fed a fat-rich meal. The stomach contained very little activity, however, when saliva was excluded. Lipolytic activity was not found in the stomach wall or in the parotid, submandibular, and sublingual glands. The findings suggest that the lingual serous glands secrete a lipase which catalyzes in the stomach the conversion of triglyceride to partial glycerides and FFA. It is proposed that this reaction is the first step in the digestion of dietary lipid.”
Combining knowledge of lingual (salivary) lipase with the below report that a-amylase-binding bacteria in plaque are aided by salivary amylase in binding dietary starch to teeth and in promoting dental caries calls into question the claims that the existence of salivary amylase proves that humans are omnivores or herbivores rather than carnivores. The salivary evidence actually seems to point more toward carnivory/faunivory than omnivory/herbivory.
From:
Salivary a-Amylase: Role in Dental Plaque and Caries Formation Critical Reviews in Oral Biology and Medicine, 4(3/4):301-307 (1993)
http://cro.sagepub.com/content/4/3/301.full.pdf+html(emphasis mine)
"In summary, the available evidence from in vitro, animal, and human studies implicates dietary starch as a cariogenic substrate. a-Amylase bound on the surface of plaque bacteria may promote the processing of dietary starch. To obtain a more meaningful picture of the role of starch and a-amylase in the caries process, the relationships between a-amylase, a-amylase-binding bacteria in plaque, and starch intake should be assessed in caries active and inactive subjects.
Bacterial plaques having high levels of a-amylase-binding bacteria may concentrate salivary a-amylase within the plaque matrix to provide more glucose from dietary starch in close proximity to the tooth surface. Such plaques would likely be more cariogenic in the presence of starch-containing foods than plaques having low numbers of a-amylase-binding bacteria. "
Diglyceride Wikipedia, the free encyclopedia
“A diglyceride, or a diacylglycerol (DAG), is a glyceride consisting of two fatty acid chains covalently bonded to a glycerol molecule through ester linkages.”
Vegetarian Frequently Asked Questions - Ingredientswww.ivu.org/faq/ingredients.html “Mono- and diglycerides are esters of edible fat-forming acids usually of the sweet alcohol glycerin. ...”
Glycerolhttp://en.wikipedia.org/wiki/Glycerol“Glycerol is sweet-tasting and of low toxicity.”
Since diglycerides contain sweet glycerol molecules (see Staying healthy with nutrition: the complete guide to diet and nutritional, By Elson M. Haas, p. 452), I wonder if the breakdown of hydrolyzed triglyceride by lingual lipase into mostly
diglyceride and free fatty acids (FFA) (and possibly partially into glycerol and fatty acids?) could explain why suet tastes mildly sweet to me when I chew it extensively.
Still more evidence that humans are more fat-oriented than starch-oriented is this report suggesting that diglyceride-rich foods may promote weight loss in humans:
Diglyceride-Rich Foods May Promote Weight Losshttp://bastyrcenter.org/content/view/448/
Topic: raw (femented?) fish oil (Read 15819 times)