Good morning! Welcome to Neurology Grand Rounds here at Blogmocracy General Hospital. Today we are going to get all sweet and look at nutrition! Not all sugars are created equal ( 😆 ) . Please read the lecture below and make sure to be familiar with our case study, our grad-ass CJ as he is a long term study in the effects of high doses of HFCS on the human body as seen over at DoD, Dr Daedalus has done quite a detailed study on this subject. It is quite clear what a long term diet made exclusively of Cheetos and Mt Dew will do to what was an in shape human.
It is quite simple. Humans love sweets. We run on glucose. When we eat glucose, chemicals are sent out to make us feel satisfied. When we eat fructose (high fructose corn syrup) for instance, these chemicals are not released and we are not satiated and eat/drink more, thereby ingesting more calories.
The following is from Wiki and has been checked for accuracy.
Glucose (/ˈɡluːkoʊs/ or /–koʊz/; C6H12O6, also known as D-glucose, dextrose, or grape sugar) is a simple monosaccharide found in plants. It is one of the three dietary monosaccharides, along with fructose and galactose, that are absorbed directly into the bloodstream during digestion. An important carbohydrate in biology, cells use it as the primary source of energy and a metabolic intermediate. Glucose is one of the main products of photosynthesis and fuels for cellular respiration. Glucose exists in several different molecular structures, but all of these structures can be divided into two families of mirror-images (stereoisomers).
Most dietary carbohydrates contain glucose, either as their only building block, as in starch and glycogen, or together with another monosaccharide, as in sucrose and lactose.
In the lumen of the duodenum and small intestine, the glucose oligo- and polysaccharides are broken down to monosaccharides by the pancreatic and intestinal glycosidases. Other polysaccharides cannot be processed by the human intestine and require assistance by intestinal flora if they are to be broken down; the most notable exceptions are sucrose (fructose-glucose) and lactose (galactose-glucose). Glucose is then transported across the apical membrane of the enterocytes by SLC5A1, and later across their basal membrane by SLC2A2. Some of the glucose is converted to lactic acid by astrocytes, which is then utilized as an energy source by brain cells, some of the glucose is used by intestinal cells and red blood cells, while the rest reaches the liver, adipose tissue and muscle cells, where it is absorbed and stored as glycogen (under the influence of insulin). Liver cell glycogen can be converted to glucose and returned to the blood when insulin is low or absent; muscle cell glycogen is not returned to the blood because of a lack of enzymes. In fat cells, glucose is used to power reactions that synthesize some fat types and have other purposes. Glycogen is the body’s “glucose energy storage” mechanism, because it is much more “space efficient” and less reactive than glucose itself.
Fructose or fruit sugar, is a simple monosaccharide found in many plants. It is one of the three dietary monosaccharides, along with glucose and galactose, that are absorbed directly into the bloodstream during digestion. Fructose was discovered by French chemist Augustin-Pierre Dubrunfaut in 1847. Pure, dry fructose is a very sweet, white, odorless, crystalline solid and is the most water-soluble of all the sugars. From plant sources, fructose is found in honey, tree and vine fruits, flowers, berries, and most root vegetables. In plants, fructose may be present as the monosaccharide and/or as a molecular component of sucrose, which is a disaccharide.
Commercially, fructose frequently is derived from sugar cane, sugar beets, and corn and there are three commercially important forms. Crystalline fructose is the monosaccharide, dried, ground, and of high purity. The second form, high-fructose corn syrup (HFCS) is a mixture of glucose and fructose as monosaccharides. The third form, sucrose, is a compound with one molecule of glucose covalently linked to one molecule of fructose. All forms of fructose, including fruits and juices, are commonly added to foods and drinks for palatability and taste enhancement, and for browning of some foods, such as baked goods.
All three dietary monosaccharides are transported into the liver by the GLUT2 transporter. Fructose and galactose are phosphorylated in the liver by fructokinase (Km= 0.5 mM) and galactokinase (Km = 0.8 mM). By contrast, glucose tends to pass through the liver (Km of hepatic glucokinase = 10 mM) and can be metabolised anywhere in the body. Uptake of fructose by the liver is not regulated by insulin. However, insulin is capable of increasing the abundance and functional activity of GLUT5 in skeletal muscle cells.
From My Medscape Account:
Fructose Effects in Brain May Contribute to Overeating
Jan 02, 2013Consuming fructose appears to cause changes in the brain that may lead to overeating, a new study suggests.
“Increases in fructose consumption have paralleled the increasing prevalence of obesity, and high-fructose diets are thought to promote weight gain and insulin resistance,” lead author Kathleen A. Page, MD, and colleagues from Yale University in New Haven, Connecticut, write.
In this study, they showed in healthy volunteers that although glucose ingestion resulted in reduced activation of the hypothalamus, insula, and striatum on MRI — areas that regulate appetite, motivation, and reward processing — as well as increased functional connections between the hypothalamic striatal network and increased satiety. Fructose ingestion had none of these effects.
“The disparate responses to fructose were associated with reduced systemic levels of the satiety-signaling hormone insulin and were not likely attributable to an inability of fructose to cross the blood-brain barrier into the hypothalamus or to a lack of hypothalamic expression of genes necessary for fructose metabolism,” they conclude.
Their findings are published in the January 2 issue of the Journal of the American Medical Association.
Glucose vs Fructose
Fructose ingestion produces smaller increases in circulating satiety hormones compared with glucose ingestion, and central administration of fructose provokes feeding in rodents, whereas centrally administered glucose promotes satiety, the authors write. “Thus, fructose possibly increases food-seeking behavior and increases food intake.”
In this study, the researchers used arterial spin labeling MRI to quantify regional cerebral blood flow in 20 healthy normal-weight adult volunteers before and after drinking a 75-g beverage of pure glucose or fructose.
They observed that glucose (but not fructose) ingestion reduced activation of the hypothalamus, insula, and striatum. Glucose ingestion also increased functional connections between the hypothalamic-striatal network and increased ratings of satiety and fullness.
Brain responses were markedly different after ingestion of an equal amount of fructose. Not only did fructose fail to diminish hypothalamic activity, but it also induced a small, transient increase in hypothalamic activity.
The striatum, as with the hypothalamus, also did not deactivate with fructose ingestion, which may cause decreased inhibitory responses. Fructose ingestion was also associated with reduced systemic levels of the satiety-signaling hormone insulin.
“These findings support the conceptual framework that when the human brain is exposed to fructose, neurobiological pathways involved in appetite regulation are modulated, thereby promoting increased food intake,” Jonathan Q. Purnell, MD, and Damien A. Fair, PhD, from Oregon Health & Science University, Portland, write in an accompanying editorial.
They say the implications of this study, coupled with mounting evidence from epidemiologic, metabolic feeding, and animal studies, are that the “advances in food processing and economic forces leading to increased intake of added sugar and accompanying fructose in U.S. society are indeed extending the supersizing concept to the population’s collective waistlines.”
The study was supported in part by grants from the National Institutes of Health and the Yale Center for Clinical Investigation. The authors and editorialists have disclosed no relevant financial relationships.