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"Syrup"
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From maple tree to syrup
Looks at the process behind the making of maple syrup, from planting the sugar maple trees through installing the spouts, collecting the sap, boiling it down to syrup, packaging the syrup, and finally eating the syrup on pancakes.
Book
Dietary fructose improves intestinal cell survival and nutrient absorption
Fructose consumption is linked to the rising incidence of obesity and cancer, which are two of the leading causes of morbidity and mortality globally
1
,
2
. Dietary fructose metabolism begins at the epithelium of the small intestine, where fructose is transported by glucose transporter type 5 (GLUT5; encoded by
SLC2A5
) and phosphorylated by ketohexokinase to form fructose 1-phosphate, which accumulates to high levels in the cell
3
,
4
. Although this pathway has been implicated in obesity and tumour promotion, the exact mechanism that drives these pathologies in the intestine remains unclear. Here we show that dietary fructose improves the survival of intestinal cells and increases intestinal villus length in several mouse models. The increase in villus length expands the surface area of the gut and increases nutrient absorption and adiposity in mice that are fed a high-fat diet. In hypoxic intestinal cells, fructose 1-phosphate inhibits the M2 isoform of pyruvate kinase to promote cell survival
5
–
7
. Genetic ablation of ketohexokinase or stimulation of pyruvate kinase prevents villus elongation and abolishes the nutrient absorption and tumour growth that are induced by feeding mice with high-fructose corn syrup. The ability of fructose to promote cell survival through an allosteric metabolite thus provides additional insights into the excess adiposity generated by a Western diet, and a compelling explanation for the promotion of tumour growth by high-fructose corn syrup.
A high-fructose diet in mice improves the survival of intestinal epithelial cells, which leads to an increase in gut surface area, enhanced absorption of lipids and the promotion of tumour growth and obesity.
Journal Article
Bear goes sugaring
\"Learn how to make syrup the old fashioned way with the help of a friendly bear and her amusingly unhelpful accomplices Dog and Squirrel in this informative comics-style picture book.\"-- Provided by publisher.
Book
High-fructose corn syrup enhances intestinal tumor growth in mice
Excessive consumption of beverages sweetened with high-fructose corn syrup (HFCS) is associated with obesity and with an increased risk of colorectal cancer. Whether HFCS contributes directly to tumorigenesis is unclear. We investigated the effects of daily oral administration of HFCS in adenomatous polyposis coli (APC) mutant mice, which are predisposed to develop intestinal tumors. The HFCS-treated mice showed a substantial increase in tumor size and tumor grade in the absence of obesity and metabolic syndrome. HFCS increased the concentrations of fructose and glucose in the intestinal lumen and serum, respectively, and the tumors transported both sugars. Within the tumors, fructose was converted to fructose-1-phosphate, leading to activation of glycolysis and increased synthesis of fatty acids that support tumor growth. These mouse studies support the hypothesis that the combination of dietary glucose and fructose, even at a moderate dose, can enhance tumorigenesis.
Journal Article
Maple syrup from the sugarhouse
Kelsey and her father begin tapping sugar maple trees as family and friends gather to help in the process of turning the harvested sap into maple syrup.
Book
Phosphatase activity-based PPM1K: a key player in the regulation of mitochondrial function and its multifaceted impact in diseases
PPM1K is a significant metal-dependent phosphatase predominantly located in the mitochondrial matrix, where it plays a crucial role in the metabolism of branched-chain amino acids (BCAAs). It is implicated in cellular function and development across various tissues and is associated with diseases like Alzheimer's, cardiomyopathy, and maple syrup urine disease (MSUD). This article reviews PPM1K's impact on mitochondrial function and cellular metabolism, as well as its role in disease progression. The regulation of PPM1K expression and activity by various factors is complex and highlights its therapeutic potential. PPM1K's dysfunction can lead to the accumulation of BCAAs and the excessive opening of the mitochondrial permeability transition pore (MPTP), disrupting physiological metabolism and function. It also regulates the degradation of BCAAs by acting as a specific phosphatase for the E1α subunit of the BCKD complex. Outside the mitochondria, PPM1K suppresses de novo fatty acid synthesis and promotes fatty acid oxidation by dephosphorylating ACL. Furthermore, PPM1K has anti-inflammatory effects and modulates immune cell infiltration in tumor tissues. The expression and activity of PPM1K are influenced by factors such as BCAA concentration, fructose intake, and drug treatments, making it a promising target for therapeutic applications and further basic research.
Journal Article
Branched-Chain Amino Acids and Brain Metabolism
This review aims to provide a historical reference of branched-chain amino acid (BCAA) metabolism and provide a link between peripheral and central nervous system (CNS) metabolism of BCAAs. Leucine, isoleucine, and valine (Leu, Ile, and Val) are unlike most other essential amino acids (AA), being transaminated initially in extrahepatic tissues, and requiring interorgan or intertissue shuttling for complete catabolism. Within the periphery, BCAAs are essential AAs and are required for protein synthesis, and are key nitrogen donors in the form of Glu, Gln, and Ala. Leucine is an activator of the mammalian (or mechanistic) target of rapamycin, the master regulator of cell growth and proliferation. The tissue distribution and activity of the catabolic enzymes in the peripheral tissues as well as neurological effects in Maple Syrup Urine Disease (MSUD) show the BCAAs have a role in the CNS. Interestingly, there are significant differences between murine and human CNS enzyme distribution and activities. In the CNS, BCAAs have roles in neurotransmitter synthesis, protein synthesis, food intake regulation, and are implicated in diseases. MSUD is the most prolific disease associated with BCAA metabolism, affecting the branched-chain α-keto acid dehydrogenase complex (BCKDC). Mutations in the branched-chain aminotransferases (BCATs) and the kinase for BCKDC also result in neurological dysfunction. However, there are many questions of BCAA metabolism in the CNS (as well as the periphery) that remain elusive. We discuss areas of BCAA and BCKA metabolism that have yet to be researched adequately.
Journal Article
Dietary fructose enhances tumour growth indirectly via interorgan lipid transfer
Fructose consumption has increased considerably over the past five decades, largely due to the widespread use of high-fructose corn syrup as a sweetener
1
. It has been proposed that fructose promotes the growth of some tumours directly by serving as a fuel
2
,
3
. Here we show that fructose supplementation enhances tumour growth in animal models of melanoma, breast cancer and cervical cancer without causing weight gain or insulin resistance. The cancer cells themselves were unable to use fructose readily as a nutrient because they did not express ketohexokinase-C (KHK-C). Primary hepatocytes did express KHK-C, resulting in fructolysis and the excretion of a variety of lipid species, including lysophosphatidylcholines (LPCs). In co-culture experiments, hepatocyte-derived LPCs were consumed by cancer cells and used to generate phosphatidylcholines, the major phospholipid of cell membranes. In vivo, supplementation with high-fructose corn syrup increased several LPC species by more than sevenfold in the serum. Administration of LPCs to mice was sufficient to increase tumour growth. Pharmacological inhibition of ketohexokinase had no direct effect on cancer cells, but it decreased circulating LPC levels and prevented fructose-mediated tumour growth in vivo. These findings reveal that fructose supplementation increases circulating nutrients such as LPCs, which can enhance tumour growth through a cell non-autonomous mechanism.
Dietary fructose enhances tumour growth in animal models of melanoma, breast cancer and cervical cancer indirectly via metabolite transfer.
Journal Article
Ultra-processed foods: what they are and how to identify them
The present commentary contains a clear and simple guide designed to identify ultra-processed foods. It responds to the growing interest in ultra-processed foods among policy makers, academic researchers, health professionals, journalists and consumers concerned to devise policies, investigate dietary patterns, advise people, prepare media coverage, and when buying food and checking labels in shops or at home. Ultra-processed foods are defined within the NOVA classification system, which groups foods according to the extent and purpose of industrial processing. Processes enabling the manufacture of ultra-processed foods include the fractioning of whole foods into substances, chemical modifications of these substances, assembly of unmodified and modified food substances, frequent use of cosmetic additives and sophisticated packaging. Processes and ingredients used to manufacture ultra-processed foods are designed to create highly profitable (low-cost ingredients, long shelf-life, emphatic branding), convenient (ready-to-consume), hyper-palatable products liable to displace all other NOVA food groups, notably unprocessed or minimally processed foods. A practical way to identify an ultra-processed product is to check to see if its list of ingredients contains at least one item characteristic of the NOVA ultra-processed food group, which is to say, either food substances never or rarely used in kitchens (such as high-fructose corn syrup, hydrogenated or interesterified oils, and hydrolysed proteins), or classes of additives designed to make the final product palatable or more appealing (such as flavours, flavour enhancers, colours, emulsifiers, emulsifying salts, sweeteners, thickeners, and anti-foaming, bulking, carbonating, foaming, gelling and glazing agents).
Journal Article
Arterial stiffness is not acutely modified by consumption of a caffeinated soft drink sweetened with high‐fructose corn syrup in young healthy adults
We tested the hypothesis that ingestion of a caffeinated soft drink sweetened with high‐fructose corn syrup acutely increases arterial stiffness. In a randomized counterbalanced, crossover design, fourteen healthy adults (25 ± 3 years, 6 women) reported to the laboratory for two experimental visits where 500 ml of tap water (H2O) or 500 ml of Mountain Dew® (a caffeinated soft drink sweetened with high‐fructose corn syrup (HFCS)) were consumed. Arterial stiffness (carotid‐to‐femoral pulse wave velocity (cfPWV)), peripheral and central blood pressures were measured pre‐consumption, 30 min post‐consumption, and 120 min post‐consumption. Prior to each measurement period, beat‐to‐beat hemodynamic measures were collected. Changes in heart rate, blood pressure, and cardiac output from pre‐consumption did not differ between trials at any timepoint (p ≥ 0.06). Moreover, changes in peripheral or central blood pressures from pre‐consumption did not differ between trials (p ≥ 0.84). Likewise, changes in cfPWV from pre‐consumption to 30 min post‐consumption (HFCS: 0.2 ± 0.3 m/s, H2O: 0.0 ± 0.3 m/s, p = 0.34) and 120 min post‐consumption (HFCS: 0.3 ± 0.4 m/s, H2O: 0.2 ± 0.3 m/s, p = 0.77) did not differ. Changes in aortic augmentation pressure, augmentation index, augmentation index corrected to a heart rate of 75 bpm, and reflection magnitude did not differ between conditions at 30 min post‐ (p ≥ 0.55) or 120 min post‐ (p ≥ 0.18) consumption. In healthy young adults, ingesting 500 ml of a commercially available caffeinated soft drink sweetened with high‐fructose corn syrup does not acutely change indices of arterial stiffness and wave reflection. This study investigated whether the ingestion of a caffeinated soft drink sweetened with high‐fructose corn syrup acutely modified arterial stiffness. In a randomized counterbalanced, crossover design, fourteen young healthy adults consumed 500 ml of tap water or a caffeinated soft drink sweetened with high‐fructose corn syrup, after which carotid‐to‐femoral pulse wave velocity was measured. This study found that ingesting 500 ml of a commercially available caffeinated soft drink sweetened with high‐fructose corn syrup does not acutely change indices of arterial stiffness.
Journal Article