The true prevalence, however, remains uncertain because of a lack of population-based studies and inconsistent criteria to define gastroparesis, including variations in the technique used to quantify ...gastric emptying (where scintigraphy remains the gold standard method and stable isotope breath tests and ultrasonography represent acceptable alternatives), the desirable blood glucose levels during the emptying measurement, the magnitude of the delay in gastric emptying regarded as abnormal, and whether the presence of gastrointestinal symptoms represents a prerequisite for the diagnosis. ...in an individual type 2 diabetic patient, the impact of a GLP-1 agonist on postprandial glycemia is likely to be dependent on both the baseline rate of emptying and the choice of GLP-1 agonist.
•Potassium release from combusting biomass studied with flame emission spectroscopy.•Biomass ash with differing quantities of an additive investigated.•3 different biomass fuels examined; softwood, ...wheat straw and olive residue.•The additive decreased K-release profiles for all biomass.•Softwood shows a high K-release rate relative to the small quantity of K in this fuel.
This study focuses on the effects of an aluminosilicate additive on the fate of potassium during biomass combustion. Such additives have shown some success in mitigating slagging and fouling problems in boilers and furnaces, and the mobility of potassium in combustion systems is one of the key factors dictating ash behaviour. To investigate this, a flame emission spectroscopy technique was used to evaluate the differences in the gas-phase potassium release profiles during the combustion of 5 mm diameter pellets of different biomass suspended in a methane-air flame. The biomass pellets were evaluated with various mixes of an aluminosilicate based additive (5, 15 and 25 wt%). Potassium emission detection, coupled with high speed video of the combustion process, indicated that potassium evolves over the three stages of volatile combustion (a sharp peak in the emission profile), char combustion (a broader peak) and “ash cooking” (a very broad peak over an extended period, long after the end of combustion). In the absence of additive, the three biomass studied (softwood, wheat straw, olive residue) behaved quite differently in terms of potassium release profiles. When the results are normalized for the amount of potassium in the fuel, it is clear that a large fraction of potassium enters the gas phase during the volatile and char combustion of the softwood. Olive residue, releases a lower fraction of potassium during the volatile and char combustion stages, indicating that more potassium is fixed in the ash. In contrast, wheat straw shows a release of potassium during combustion, and then, after a period of “ash cooking”, a substantial gradual release with continued exposure to hot combustion gases. The difference in the emission profiles can be interpreted in terms of the K:Cl ratios and the K:(Si + Al) ratios: high chlorine and/or low (Si + Al) facilitates the release of KCl or KOH to the gas phase, while high (Si + Al) helps to fix K in the solid phase. The addition of the aluminosilicate additive shows a clear reduction in the potassium released from all the biomass pellets, particularly during the char-oxidation and “ash cooking” stages, and the level of additive required is related to the amount of K in the biomass. The potassium emission experiments were complemented by laboratory-scale preparation of ash at different temperatures, and detection of residual potassium in the ash using Atomic Absorption Spectroscopy (AAS). These results validated the findings and quantified the higher fractions of potassium retained within the ash when additives are used. For the wood ash 70–100% of K is retained in the ash in the presence of additive; for the wheat straw, this figure is 60–80% and for the olive pellets it is 70–100%.
There is much concern about the toxicological effects of synthetic hair dyes. As an alternative approach, renewable waste blackcurrant (Ribes nigrum L.) fruit skins from the fruit pressing industry ...were extracted using acidified water with a solid-phase purification stage. Anthocyanin colorants were isolated in good yields (2–3% w/w) and characterized by HPLC. Sorption of anthocyanins onto hair followed a Freundlich isotherm; anthocyanin–anthocyanin aggregation interactions enabled high buildup on the substrate. Sorption energy of cyanidin-3-O-glucoside (monosaccharide) > cyanidin-3-O-rutinoside (disaccharide), but sorption properties of different anthocyanin glucosides were very similar. Intense blue-colored dyeing on hair could be achieved with λmax‑vis at 580 nm, typical of the anionic quinonoid base; it is suggested that hair provides an environment that enables the stabilization of the anionic quinonoid base on adsorption through association with cations in the hair and copigmentation effects. Dyeings were stable to multiple washes.
GLP-1 and glucose-dependent insulinotropic polypeptide (GIP), which are released from the intestines after meals, are responsible for augmenting insulin secretion (ie, the incretin effect). Because ...the insulinotropic effect of GIP is markedly attenuated in type 2 diabetes, therapeutic development to date has focused on GLP-1, which also lowers blood glucose by suppressing glucagon and energy intake, and slowing gastric emptying.1 Use of GLP-1 receptor agonists for the management of type 2 diabetes is increasing rapidly, and is associated with weight loss, negligible risk of hypoglycaemia, and potential cardiovascular protection. ...how much does GIP receptor stimulation contribute to the effects of tirzepatide? GIP has incompletely understood effects on adipose tissue, intestinal blood flow, glucagon secretion, and even bone resorption; moreover, its insulinotropic effect can be restored, in part, with fastidious glycaemic control.8 Historically, the evaluation of GIP actions has been hampered by species differences, but a human GIP receptor antagonist is now available, and should be used in future mechanistic studies.9 Second, does persistent slowing of gastric emptying by GLP-1 receptor stimulation contribute to the substantial reductions in postprandial glycaemia by tirzepatide? ...the positioning of tirzepatide in the therapeutic algorithm will be influenced by emerging information on cardiovascular outcomes, fatty liver disease, renal protection, and durability of effects, which is awaited with interest.
Type 2 diabetes mellitus (T2DM) is an increasingly prevalent chronic condition, characterized by abnormally elevated blood glucose concentrations and, as a consequence, increased risk of micro‐ and ...macrovascular complications. Metformin is usually the first‐line glucose‐lowering medication in T2DM; however, despite being used for more than 60 years, the mechanism underlying the glucose‐lowering action of metformin remains incompletely understood. Although metformin reduces hepatic glucose production, there is persuasive evidence that the gastrointestinal tract is crucial in mediating this effect, particularly via secretion of the incretin hormone glucagon‐like peptide 1 (GLP‐1). It is now well recognized that bile acids, in addition to their established function in fat digestion and absorption, are important regulators of glucose metabolism. Exposure of the small and large intestine to bile acids induces GLP‐1 secretion, modulates the composition of the gut microbiota, and reduces postprandial blood glucose excursions in humans with and without T2DM. Metformin reduces intestinal bile acid resorption substantially, such that intraluminal bile acids may, at least in part, account for its glucose‐lowering effect. The present review focuses on the conceptual shift in our understanding as to how metformin lowers blood glucose in T2DM, with a particular emphasis on the role of intestinal bile acids.
Gastric emptying is a major determinant of postprandial blood glucose, accounting for ~35% of variance in peak glucose in both healthy individuals and those with type 2 diabetes. Gastric emptying is ...frequently disordered in individuals with diabetes (both abnormally delayed and accelerated). Delayed gastric emptying, i.e. diabetic gastroparesis, may be linked to upper gastrointestinal symptoms for which current treatment remains suboptimal; pharmacological acceleration of delayed emptying is only weakly associated with symptom improvement. Accordingly, the relationship between symptoms and delayed gastric emptying is not simply ‘cause and effect’. In insulin-treated patients, disordered gastric emptying, even when not associated with gastrointestinal symptoms, can cause a mismatch between the onset of insulin action and the availability of absorbed carbohydrate, leading to suboptimal glycaemic control. In patients with type 2 diabetes, interventions that slow gastric emptying, e.g. glucagon-like peptide-1 receptor agonists, reduce postprandial blood glucose. This review focuses on recent insights into the impact of gastric emptying on postprandial blood glucose, effects of diabetes therapy on gastric emptying and the management of disordered gastric emptying in diabetes. In view of the broad relevance of gastric emptying to diabetes management, it is important that future clinical trials evaluating novel therapies that may affect gastric emptying should quantify the latter with an appropriate technique, such as scintigraphy or a stable isotope breath test.
Graphical abstract
Intestinal glucose stimulates secretion of the incretin hormone glucagon-like peptide 1 (GLP-1). The mechanisms underlying this pathway have not been fully investigated in humans. In this study, we ...showed that a 30-min intraduodenal glucose infusion activated half of all duodenal L cells in humans. This infusion was sufficient to increase plasma GLP-1 levels. With an ex vivo model using human gut tissue specimens, we showed a dose-responsive GLP-1 secretion in the ileum at ≥200 mmol/L glucose. In ex vivo tissue from the duodenum and ileum, but not the colon, 300 mmol/L glucose potently stimulated GLP-1 release. In the ileum, this response was independent of osmotic influences and required delivery of glucose via GLUT2 and mitochondrial metabolism. The requirement of voltage-gated Na
and Ca
channel activation indicates that membrane depolarization occurs. K
channels do not drive this, as tolbutamide did not trigger release. The sodium-glucose cotransporter 1 (SGLT1) substrate α-MG induced secretion, and the response was blocked by the SGLT1 inhibitor phlorizin or by replacement of extracellular Na
with
-methyl-d-glucamine. This is the first report of the mechanisms underlying glucose-induced GLP-1 secretion from human small intestine. Our findings demonstrate a dominant role of SGLT1 in controlling glucose-stimulated GLP-1 release in human ileal L cells.
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