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Using this guide, you can design a low-carb, low-calorie diet that helps you shed weight while controlling your diabetes. --from publisher description.

Abstract Context Meal timing affects metabolic homeostasis and body weight, but how composition and timing of meals affect plasma lipidomics in humans is not well studied. Objective We used high throughput shotgun plasma lipidomics to investigate effects of timing of carbohydrate and fat intake on lipid metabolism and its relation to glycemic control. Design 29 nondiabetic men consumed (1) a high-carb test meal (MTT-HC) at 09.00 and a high-fat meal (MTT-HF) at 15.40; or (2) MTT-HF at 09.00 and MTT-HC at 15.40. Blood was sampled before and 180 minutes after completion of each MTT. Subcutaneous adipose tissue (SAT) was collected after overnight fast and both MTTs. Prior to each investigation day, participants consumed a 4-week isocaloric diet of the same composition: (1) high-carb meals until 13.30 and high-fat meals between 16.30 and 22:00 or (2) the inverse order. Results 12 hour daily lipid patterns showed a complex regulation by both the time of day (67.8%) and meal composition (55.4%). A third of lipids showed a diurnal variation in postprandial responses to the same meal with mostly higher responses in the morning than in the afternoon. Triacylglycerols containing shorter and more saturated fatty acids were enriched in the morning. SAT transcripts involved in fatty acid synthesis and desaturation showed no diurnal variation. Diurnal changes of 7 lipid classes were negatively associated with insulin sensitivity, but not with glucose and insulin response or insulin secretion. Conclusions This study identified postprandial plasma lipid profiles as being strongly affected by meal timing and associated with insulin sensitivity.

The carbohydrate–insulin model of obesity posits that high-carbohydrate diets lead to excess insulin secretion, thereby promoting fat accumulation and increasing energy intake. Thus, low-carbohydrate diets are predicted to reduce ad libitum energy intake as compared to low-fat, high-carbohydrate diets. To test this hypothesis, 20 adults aged 29.9 ± 1.4 (mean ± s.e.m.) years with body mass index of 27.8 ± 1.3 kg m −2 were admitted as inpatients to the National Institutes of Health Clinical Center and randomized to consume ad libitum either a minimally processed, plant-based, low-fat diet (10.3% fat, 75.2% carbohydrate) with high glycemic load (85 g 1,000 kcal −1 ) or a minimally processed, animal-based, ketogenic, low-carbohydrate diet (75.8% fat, 10.0% carbohydrate) with low glycemic load (6 g 1,000 kcal −1 ) for 2 weeks followed immediately by the alternate diet for 2 weeks. One participant withdrew due to hypoglycemia during the low-carbohydrate diet. The primary outcomes compared mean daily ad libitum energy intake between each 2-week diet period as well as between the final week of each diet. We found that the low-fat diet led to 689 ± 73 kcal d −1 less energy intake than the low-carbohydrate diet over 2 weeks ( P  < 0.0001) and 544 ± 68 kcal d −1 less over the final week ( P  < 0.0001). Therefore, the predictions of the carbohydrate–insulin model were inconsistent with our observations. This study was registered on ClinicalTrials.gov as NCT03878108 . In an inpatient, randomized controlled crossover trial, participants consumed 550–700 kcal day −1 fewer calories when following a plant-based, low-fat diet with a high glycemic load compared with an animal-based, low-carbohydrate diet with a low glycemic load; weight loss was comparable between the two diets and there were no significant differences in hunger or enjoyment of the meals.

Lactiplantibacillus plantarum has a strong carbohydrate utilization ability. This characteristic plays an important role in its gastrointestinal tract colonization and probiotic effects. L. plantarum LP-F1 presents a high carbohydrate utilization capacity. The genome analysis of 165 L. plantarum strains indicated the species has a plenty of carbohydrate metabolism genes, presenting a strain specificity. Furthermore, two-component systems (TCSs) analysis revealed that the species has more TCSs than other lactic acid bacteria, and the distribution of TCS also shows the strain specificity. In order to clarify the sugar metabolism mechanism under different carbohydrate fermentation conditions, the expressions of 27 carbohydrate metabolism genes, catabolite control protein A (CcpA) gene ccpA, and TCSs genes were analyzed by quantitative real-time PCR technology. The correlation analysis between the expressions of regulatory genes and sugar metabolism genes showed that some regulatory genes were correlated with most of the sugar metabolism genes, suggesting that some TCSs might be involved in the regulation of sugar metabolism.

Carbohydrate supplementation optimises athletic performance, but the metabolic and performance impacts of commercial products/compositions are underexplored. We compared the efficacy of three commercial carbohydrate supplements: a glucose–fructose bar (GF‐Bar), a glucose–fructose hydrogel (GF‐Gel) and a maltodextrin‐based gel (MD‐Gel). Antegrade venous blood samples for glucose and insulin were measured alongside substrate utilisation in healthy Tier 2 athletes after ingesting 45 g of carbohydrates from the GF‐Bar, GF‐Gel and MD‐Gel during a modified 1‐h oral glucose tolerance test (OGTT). Additionally, the effect of supplementation on high‐intensity interval exercise was evaluated during repeated maximal sprint performance. During the OGTT, the GF‐Bar elicited greater total carbohydrate oxidation than MD‐Gel (24.6 ± 7.4 g vs. 17.8 ± 8.6 g, P = 0.038) but not GF‐Gel (20.1 ± 6.4 g, P > 0.05). Carbohydrate oxidation per minute varied over time (P < 0.001) and between products (P = 0.043), with GF‐Bar (0.27 ± 0.05 g min−1) showing higher oxidation than GF‐Gel (0.21 ± 0.05 g min−1) and MD‐Gel (0.19 ± 0.06 g min−1). No differences were observed in glucose peak, time to peak glucose or insulin concentration (P > 0.05). Peak power (P = 0.011), mean power (P < 0.001) and total work varied across sprints (P < 0.001) but not between products (P > 0.05). Perceived exertion and gastrointestinal discomfort were similar between products (P > 0.05). Despite differences in carbohydrate oxidation during the OGTT, the GF‐Bar, GF‐Gel and MD‐Gel displayed similar metabolic and sprint performance outcomes, suggesting that, within this study, carbohydrate formulation did not impact short‐duration maximal exercise. What is the central question of this study? Carbohydrate supplementation optimises athletic performance, but the metabolic and performance impacts of commercial products/compositions are underexplored: what is the efficacy of a glucose–fructose bar, a glucose–fructose hydrogel and a maltodextrin‐based gel? What is the main finding and its importance? In Tier 2 athletes, a glucose–fructose bar led to significantly greater total carbohydrate oxidation than a maltodextrin gel during a 1‐h OGTT but not compared to a glucose–fructose hydrogel. No significant effects were observed on blood glucose, insulin, sprint performance or gastrointestinal comfort. All supplements produced similar outcomes during repeated high‐intensity sprints, suggesting that carbohydrate formulation did not influence short‐duration maximal exercise performance in this context.

Haploinsufficiency of the SLC2A1 gene and paucity of its translated product, the glucose transporter-1 (Glut1) protein, disrupt brain function and cause the neurodevelopmental disorder, Glut1 deficiency syndrome (Glut1 DS). There is little to suggest how reduced Glut1 causes cognitive dysfunction and no optimal treatment for Glut1 DS. We used model mice to demonstrate that low Glut1 protein arrests cerebral angiogenesis, resulting in a profound diminution of the brain microvasculature without compromising the blood–brain barrier. Studies to define the temporal requirements for Glut1 reveal that pre-symptomatic, AAV9-mediated repletion of the protein averts brain microvasculature defects and prevents disease, whereas augmenting the protein late, during adulthood, is devoid of benefit. Still, treatment following symptom onset can be effective; Glut1 repletion in early-symptomatic mutants that have experienced sustained periods of low brain glucose nevertheless restores the cerebral microvasculature and ameliorates disease. Timely Glut1 repletion may thus constitute an effective treatment for Glut1 DS. Glut1-deficiency syndrome is a severe neurodevelopmental disorder characterized by low brain glucose and epileptic seizures. Tang et al . show that in model mice, low Glut1 leads to defects of the brain vasculature, and that AAV9-based gene therapy at pre- or early-symptomatic stages prevents the defects and mitigates disease.

Carbohydrate metabolism is essential for cellular energy balance as well as for the biosynthesis of new cellular building blocks. As animal nutrient intake displays temporal fluctuations and each cell type within the animal possesses specific metabolic needs, elaborate regulatory systems are needed to coordinate carbohydrate metabolism in time and space. Carbohydrate metabolism is regulated locally through gene regulatory networks and signaling pathways, which receive inputs from nutrient sensors as well as other pathways, such as developmental signals. Superimposed on cell-intrinsic control, hormonal signaling mediates intertissue information to maintain organismal homeostasis. Misregulation of carbohydrate metabolism is causative for many human diseases, such as diabetes and cancer. Recent work in has uncovered new regulators of carbohydrate metabolism and introduced novel physiological roles for previously known pathways. Moreover, genetically tractable models to study carbohydrate metabolism-related human diseases have provided new insight into the mechanisms of pathogenesis. Due to the high degree of conservation of relevant regulatory pathways, as well as vast possibilities for the analysis of gene-nutrient interactions and tissue-specific gene function, is emerging as an important model system for research on carbohydrate metabolism.

Soil salinity increasingly causes crop losses worldwide. Although roots are the primary targets of salt stress, the signaling networks that facilitate metabolic reprogramming to induce stress tolerance are less understood than those in leaves. Here, a combination of transcriptomic and metabolic approaches was performed in salt-treated Arabidopsis thaliana roots, which revealed that the group S1 basic leucine zipper transcription factors bZIP1 and bZIP53 reprogram primary C- and N-metabolism. In particular, gluconeogenesis and amino acid catabolism are affected by these transcription factors. Importantly, bZIP1 expression reflects cellular stress and energy status in roots. In addition to the well-described abiotic stress response pathway initiated by the hormone abscisic acid (ABA) and executed by SnRK2 (Snf1-RELATED-PROTEIN-KINASE2) and AREB-like bZIP factors, we identify a structurally related ABA-independent signaling module consisting of SnRK1s and S1 bZIPs. Crosstalk between these signaling pathways recruits particular bZIP factor combinations to establish at least four distinct gene expression patterns. Understanding this signaling network provides a framework for securing future crop productivity.

This study evaluated the effects of chenodeoxycholic acid (CDCA), a farnesoid X receptor (FXR) potential activator, on growth performance, antioxidant capacity, glucose metabolism and inflammation in largemouth bass (Micropterus salmoides) (initial body weight: 5·45 ± 0·02 g) fed a high-carbohydrate diet. Experimental diets included a positive control (5 % α-starch), a negative control (10 % α-starch) and two diets containing 10 % α-starch supplemented with either 0·05 % or 0·10 % CDCA. After 8 weeks, the high-carbohydrate diet reduced growth performance and increased hepatosomatic and viscerosomatic indexes, which were mitigated by 0·10 % CDCA supplementation. The high-carbohydrate diet also increased hepatic glycogen and crude lipid content, both of which were reduced by 0·10 % CDCA. Furthermore, the high-carbohydrate diet-induced oxidative stress, histopathological changes and reduced liver lysozyme activity, which were ameliorated by CDCA supplementation. Molecular analysis showed that the high-carbohydrate diet suppressed FXR and phosphorylated AKT1 (p-AKT1) protein expression in the liver, downregulated insulin signalling (ira, irs, pi3kr1 and akt1), gluconeogenesis (pepck and g6pc) and glycolysis genes (gk, pk and pfkl). CDCA supplementation upregulated fxr expression, activated shp, enhanced the expression of insulin signalling and glycolytic genes (gk, pk and pfkl) and inhibited gluconeogenesis. Additionally, CDCA reduced inflammatory markers (nf-κb and il-1β) and restored anti-inflammatory mediators (il-10, iκb and tgf-β). In conclusion, 0·10 % CDCA improved carbohydrate metabolism and alleviated liver inflammation in largemouth bass fed a high dietary carbohydrate, partially through FXR activation.

Triphenyl phosphate is a high production volume organophosphate flame retardant that has been detected in multiple environmental media at increasing concentrations. The environmental and health risks of triphenyl phosphate have drawn attention because of the multiplex toxicity of this chemical compound. However, few studies have paid close attention to the impacts of triphenyl phosphate on liver metabolism. We investigated hepatic histopathological, metabolomic and transcriptomic responses of zebrafish after exposure to 0.050 mg/L and 0.300 mg/L triphenyl phosphate for 7 days. Metabolomic analysis revealed significant changes in the contents of glucose, UDP-glucose, lactate, succinate, fumarate, choline, acetylcarnitine, and several fatty acids. Transcriptomic analysis revealed that related pathways, such as the glycosphingolipid biosynthesis, PPAR signaling pathway and fatty acid elongation, were significantly affected. These results suggest that triphenyl phosphate exposure markedly disturbs hepatic carbohydrate and lipid metabolism in zebrafish. Moreover, DNA replication, the cell cycle, and non-homologous end-joining and base excision repair were strongly affected, thus indicating that triphenyl phosphate hinders the DNA damage repair system in zebrafish liver cells. The present study provides a systematic analysis of the triphenyl phosphate-induced toxic effects in zebrafish liver and demonstrates that low concentrations of triphenyl phosphate affect normal metabolism and cell cycle.