Risk of insulin resistance, impaired glycemic control, and cardiovascular disease is excessive in overweight and obese populations. We hypothesized that increasing expression of glyoxalase 1 (Glo1)-an enzyme that catalyzes the metabolism of reactive metabolite and glycating agent methylglyoxal-may improve metabolic and vascular health. Dietary bioactive compounds were screened for Glo1 inducer activity in a functional reporter assay, hits were confirmed in cell culture, and an optimized Glo1 inducer formulation was evaluated in a randomized, placebo-controlled crossover clinical trial in 29 overweight and obese subjects. We found trans-resveratrol (tRES) and hesperetin (HESP), at concentrations achieved clinically, synergized to increase Glo1 expression. In highly overweight subjects (BMI >27.5 kg/m 2 ), tRES-HESP coformulation increased expression and activity of Glo1 (27%, P < 0.05) and decreased plasma methylglyoxal (237%, P < 0.05) and total body methylglyoxal-protein glycation (214%, P < 0.01). It decreased fasting and postprandial plasma glucose (25%, P < 0.01, and 28%, P < 0.03, respectively), increased oral glucose insulin sensitivity index (42 mL $ min 21 $ m 22, P < 0.02), and improved arterial dilatation Dbrachial artery flowmediated dilatation/Ddilation response to glyceryl nitrate (95% CI 0.13-2.11). In all subjects, it decreased vascular inflammation marker soluble intercellular adhesion molecule-1 (210%, P < 0.01). In previous clinical evaluations, tRES and HESP individually were ineffective. tRES-HESP coformulation could be a suitable treatment for improved metabolic and vascular health in overweight and obese populations.
Summary• Recent studies demonstrating an in situ formation of methane (CH 4 ) within foliage and separate observations that soil-derived CH 4 can be released from the stems of trees have continued the debate about the role of vegetation in CH 4 emissions to the atmosphere. Here, a study of the role of ultraviolet (UV) radiation in the formation of CH 4 and other trace gases from plant pectins in vitro and from leaves of tobacco (Nicotiana tabacum) in planta is reported.• Plant pectins were investigated for CH 4 production under UV irradiation before and after de-methylesterification and with and without the singlet oxygen scavenger 1,4-diazabicyclo[2.2.2]octane (DABCO). Leaves of tobacco were also investigated under UV irradiation and following leaf infiltration with the singlet oxygen generator rose bengal or the bacterial pathogen Pseudomonas syringae.• Results demonstrated production of CH 4 , ethane and ethylene from pectins and from tobacco leaves following all treatments, that methyl-ester groups of pectin are a source of CH 4 , and that reactive oxygen species (ROS) arising from environmental stresses have a potential role in mechanisms of CH 4 formation.• Rates of CH 4 production were lower than those previously reported for intact plants in sunlight but the results clearly show that foliage can emit CH 4 under aerobic conditions.
Ultraviolet (UV) radiation has recently been demonstrated to drive an aerobic production of methane (CH4) from plant tissues and pectins, as do agents that generate reactive oxygen species (ROS) in vivo independently of UV. As the major building-blocks of pectin do not absorb solar UV found at the earth's surface (i.e. >280 nm), we explored the hypothesis that UV radiation affects pectin indirectly via generation of ROS which themselves release CH4 from pectin. Decreasing the UV absorbance of commercial pectin by ethanol washing diminished UV-dependent CH4 production, and this was restored by the addition of the UV photosensitizer tryptophan.
The cell-wall pectic domain rhamnogalacturonan-II (RG-II) is cross-linked via borate diester bridges, which influence the expansion, thickness and porosity of the wall. Previously, little was known about the mechanism or subcellular site of this cross-linking. Using polyacrylamide gel electrophoresis (PAGE) to separate monomeric from dimeric (boron-bridged) RG-II, we confirmed that Pb2+ promotes H3BO3-dependent dimerisation in vitro. H3BO3 concentrations as high as 50 mm did not prevent cross-linking. For in-vivo experiments, we successfully cultured ‘Paul's Scarlet’ rose (Rosa sp.) cells in boron-free medium: their wall-bound pectin contained monomeric RG-II domains but no detectable dimers. Thus pectins containing RG-II domains can be held in the wall other than via boron bridges. Re-addition of H3BO3 to 3.3 μm triggered a gradual appearance of RG-II dimer over 24 h but without detectable loss of existing monomers, suggesting that only newly synthesised RG-II was amenable to boron bridging. In agreement with this, Rosa cultures whose polysaccharide biosynthetic machinery had been compromised (by carbon starvation, respiratory inhibitors, anaerobiosis, freezing or boiling) lost the ability to generate RG-II dimers. We conclude that RG-II normally becomes boron-bridged during synthesis or secretion but not post-secretion. Supporting this conclusion, exogenous [3H]RG-II was neither dimerised in the medium nor cross-linked to existing wall-associated RG-II domains when added to Rosa cultures. In conclusion, in cultured Rosa cells RG-II domains have a brief window of opportunity for boron-bridging intraprotoplasmically or during secretion, but secretion into the apoplast is a point of no return beyond which additional boron-bridging does not readily occur.
Summary• Several studies have reported in situ methane (CH 4 ) emissions from vegetation foliage, but there remains considerable debate about its significance as a global source. Here, we report a study that evaluates the role of ultraviolet (UV) radiation-driven CH 4 emissions from foliar pectin as a global CH 4 source.• We combine a relationship for spectrally weighted CH 4 production from pectin with a global UV irradiation climatology model, satellite-derived leaf area index (LAI) and air temperature data to estimate the potential global CH 4 emissions from vegetation foliage.• Our results suggest that global foliar CH 4 emissions from UV-irradiated pectin could account for 0.2-1.0 Tg yr )1 , of which 60% is from tropical latitudes, corresponding to < 0.2% of total CH 4 sources.• Our estimate is one to two orders of magnitude lower than previous estimates of global foliar CH 4 emissions. Recent studies have reported that pectin is not the only molecular source of UV-driven CH 4 emissions and that other environmental stresses may also generate CH 4 . Consequently, further evaluation of such mechanisms of CH 4 generation is needed to confirm the contribution of foliage to the global CH 4 budget.
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