Usage The food ingredient landscape is changing, with consumers shifting their focus away from specific ingredients to overall calories and nutrition.

TORONTO, ON - Hummingbird metabolism is a marvel of evolutionary engineering. These tiny birds can power all of their energetic hovering flight by burning the sugar contained in the floral nectar of their diet. Now new research from the University of Toronto Scarborough shows they are equally adept at burning both glucose and fructose, which […]

The title compound, C12H21NO7, (I), is conformationally unstable; the predominant form present in its solution is the β-pyran­ose form (74.3%), followed by the β- and α-furan­oses (12.1 and 10.2%, respectively), α-pyran­ose (3.4%), and traces of the acyclic carbohydrate tautomer. In the crystalline state, the carbohydrate part of (I) adopts the 2C5 β-pyran­ose conformation, and the amino acid portion exists as a zwitterion, with the side chain cyclo­pentane ring assuming the E9 envelope conformation. All heteroatoms are involved in hydrogen bonding that forms a system of anti­parallel infinite chains of fused R33(6) and R33(8) rings. The mol­ecule features extensive intra­molecular hydrogen bonding, which is uniquely multicentered and involves the carboxyl­ate, ammonium and carbohydrate hy­droxy groups. In contrast, the contribution of inter­molecular O⋯H/H⋯O contacts to the Hirshfeld surface is relatively low (38.4%), as compared to structures of other d-fructose-amino acids. The 1H NMR data suggest a slow rotation around the C1—C2 bond in (I), indicating that the intra­molecular heteroatom contacts survive in aqueous solution of the mol­ecule as well.

Yesterday, a report was released by Environmental Health that got me re-thinking the few foods left in my home that still contain high fructose corn syrup (HFCS

There are many issues about high-fructose corn syrup, all of them connected to corn-focused industrial agriculture, a practice that is destroying our health and

Princeton University study finds that rats get fatter on high fructose corn syrup than on sugar, even when caloric intake is the same.

Is a Princeton University study about high fructose corn syrup causing obesity in lab rats really the answer to America's obesity problem?

The makers of the sweetener have petitioned the FDA to rename it Corn Sugar in the best interest of making things clear for the consumer.

You're going to snicker at the show's take on the controversial sweetener.

This weekend, read about how high fructose corn syrup might be to blame for the bees disappearing along with a few other disturbing news items.

Food and Drug Administration denies the Corn Refiners Association's request to change the name of the famous syrup to corn sugar.

A new study finds that participants were hungrier after consuming fructose than they were after consuming glucose.

Many people would prefer that sweets contain sugar and not high-fructose corn syrup. Hershey is considering giving them what they want.

Researchers find that fructose may be more harmful than other sugars when it comes to its effect on blood sugar levels and insulin resistance.

What's wrong with high fructose corn syrup? How about obesity, mercury and environmental damage?

Excessive fructose consumption is closely linked to the pathogenesis of metabolic disease. Carbohydrate response element-binding protein (ChREBP) is a transcription factor essential for fructose tolerance in mice. However, the functional significance of liver ChREBP in fructose metabolism remains unclear. Here, we show that liver ChREBP protects mice against fructose-induced hepatotoxicity by regulating liver glycogen metabolism and ATP homeostasis. Liver-specific ablation of ChREBP did not compromise fructose tolerance, but rather caused severe transaminitis and hepatomegaly with massive glycogen overload in mice fed a high-fructose diet, while no obvious inflammation, cell death, or fibrosis was detected in the liver. In addition, liver ATP contents were significantly decreased by ChREBP deficiency in the fed state, which was rendered more pronounced by fructose feeding. Mechanistically, liver contents of glucose-6-phosphate (G6P), an allosteric activator of glycogen synthase, were markedly increased in the absence of liver ChREBP, while fasting-induced glycogen breakdown was not compromised. Furthermore, hepatic overexpression of LPK, a ChREBP target gene in glycolysis, could effectively rescue glycogen overload and ATP reduction, as well as mitigate fructose-induced hepatotoxicity in ChREBP-deficient mice. Taken together, our findings establish a critical role of liver ChREBP in coping with hepatic fructose stress and protecting from hepatotoxicity by regulating LPK.

Understanding fructose metabolism might provide insights to renal pathophysiology. To support systemic glucose concentration, the proximal tubular cells reabsorb fructose as a substrate for gluconeogenesis. However, in instances when fructose intake is excessive, fructose metabolism is costly, resulting in energy depletion, uric acid generation, inflammation, and fibrosis in the kidney. A recent scientific advance is the discovery that fructose can be endogenously produced from glucose under pathologic conditions, not only in kidney diseases, but also in diabetes, in cardiac hypertrophy, and with dehydration. Why humans have such a deleterious mechanism to produce fructose is unknown, but it may relate to an evolutionary benefit in the past. In this article, we aim to illuminate the roles of fructose as it relates to gluconeogenesis and fructoneogenesis in the kidney.

Breast cancer is a leading cause of death in women worldwide, but the underlying mechanisms of breast tumorigenesis remain unclear. Fructose-1, 6-bisphosphatase 1 (FBP1), a rate-limiting enzyme in gluconeogenesis, was recently shown to be a tumor suppressor in breast cancer. However, the mechanisms of FBP1 as a tumor suppressor in breast cancer remain to be explored. Here we showed that FBP1 bound to Notch1 in breast cancer cells. Moreover, FBP1 enhanced ubiquitination of Notch1, further leading to proteasomal degradation via FBXW7 pathway. In addition, we found that FBP1 significantly repressed the transactivation of Notch1 in breast cancer cells. Functionally, Notch1 was involved in FBP1-mediated tumorigenesis of breast cancer cells in vivo and in vitro. Totally, these findings indicate that FBP1 inhibits breast tumorigenesis by regulating Notch1 pathway, highlighting FBP1 as a potential therapeutic target for breast cancer.