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Gastrointestinal Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Gareth Davies, Chris Black, Keeley Fairbrass
Definitions of dyspepsia (or indigestion) are vague, referring to a range of upper GI symptoms including: Epigastric pain or burningEarly satietyPost-prandial fullnessNauseaBloating
Brain Insulin Action in the Control of Metabolism in Humans
Published in André Kleinridders, Physiological Consequences of Brain Insulin Action, 2023
Furthermore, research in animals indicates a role of central insulin action in the control of lipolysis in adipose tissue (113). In humans, only a few studies exist with conflicting results (4). Intranasal insulin seems to increase postprandial thermogenesis and decrease prandial free-fatty acids in healthy men (114). In response to exercise, intranasal insulin decreased fat oxidation in normal weight but not overweight participants (123). Furthermore, intranasal insulin caused a reduction in lipolysis measured by the rate of appearance of deuterated glycerol and lowers systemic levels of free-fatty acids concentrations; however, without affecting subcutaneous lipolysis (124). Moreover, other studies could not confirm this finding (25, 115, 125), which is probably related to different study designs. Hence, further research is needed to clarify potential role of the central insulin-adipocyte axis.
Diabetes mellitus and cardiovascular disease in the elderly
Published in Wilbert S. Aronow, Jerome L. Fleg, Michael W. Rich, Tresch and Aronow’s Cardiovascular Disease in the Elderly, 2019
Initial management with insulin typically involves a basal, long-acting insulin to provide steady levels of insulin during the day and night. This can be achieved with intermediate-acting insulins such as neutral protamine Hagedorn (NPH) or long-acting insulin analogs (glargine or detemir). These insulins are usually dosed at night and titrated to achieve a target morning glucose level. Oral agents such as metformin, sulfonylureas, pioglitazone, or DPP-IV inhibitors can be continued while basal insulin therapy is used but dose reductions of oral agents may be necessary. β-cell dysfunction may become so severe that basal insulin alone is not sufficient to achieve desired glycemic control. Short-acting insulins given at meal times to assist with prandial rises in glucose may be necessary. This can be achieved with rapid-acting insulin analogs such as lispro, aspart, or glulisine (123,124).
Recent developments in adjunct therapies for type 1 diabetes
Published in Expert Opinion on Investigational Drugs, 2022
Joseph G. Timmons, Lucy Littlejohn, James G. Boyle, John R. Petrie
This is the only adjunct agent currently licensed in T1D in the USA (from 2005 but not to date in Europe) and is marketed as Symlin [5,26]. It is a synthetic analogue of Amylin (otherwise known as islet amyloid polypeptide – IAPP), a 37 amino acid peptide co-secreted with insulin from pancreatic β-cells [27]. Amylin has at least four sets of actions that synergize with insulin to reduce postprandial glycemic excursions: 1) enhancing post-prandial satiety via central mechanisms thereby reducing caloric intake; 2) reducing dysfunctional glucagon secretion by pancreatic α-cells; 3) delaying gastric emptying (often dysfunctionally fast in diabetes); and 4) reducing hepatic glucose production [25,26]. In both T1D and T2D, endogenous physiological secretion of amylin is reduced [27].
Similar fat and carbohydrate oxidation in response to arm cycling exercise in persons with spinal cord injury versus able-bodied
Published in The Journal of Spinal Cord Medicine, 2022
Todd A. Astorino, David W. McMillan
A mechanism explaining the relatively low fat oxidation observed is beyond the scope of our investigation, yet several potential explanations exist. First, the intensity of this bout was relatively high despite the low power output used. At similar relative intensities (60–70%VO2peak) implemented during continuous arm cycling, Kang et al.35 reported RER ranging from 0.94–0.98 in young AB men and women with VO2peak equal to 29 mL/kg/min. Second, in comparison to the lower body, it is apparent that the upper-body has a greater ratio of type 2 fibers and lower oxidative capacity36 that enhances reliance on CHO utilization through glycolysis for ATP supply.2 Third, our data show a significant increase in BLa recorded post-exercise that may inhibit fat oxidation.2 Lastly, our participants were at least 3 h post-prandial when they performed continuous exercise which is within a duration where a prior meal could induce an increase in plasma insulin concentration and in turn, attenuate fat oxidation.37 However, previous results38 showed that pre-exercise CHO feeding did not alter fuel use during prolonged arm cycling in persons with SCI in comparison to water, so it is possible that this had little effect upon our results.
EPA’s pleiotropic mechanisms of action: a narrative review
Published in Postgraduate Medicine, 2021
John R. Nelson, Matthew J. Budoff, Omar R. Wani, Viet Le, Dhiren K. Patel, Ashley Nelson, Richard L. Nemiroff
There are several other putative mechanisms for reduced VLDL synthesis. One such mechanism is the induction of enhanced β-oxidation of free fatty acids in peroxisomes and mitochondria, thus reducing the amount of substrate available for triglyceride and VLDL synthesis [43]. EPA has also been shown to inhibit the enzymes phosphatidic acid phosphatase/phosphohydrolase and diacylglycerol acyltransferase, involved in triglyceride synthesis [43]. EPA may also reduce triglyceride levels through increased clearance of the triglyceride-rich lipoproteins VLDL and chylomicrons via lipoprotein lipase activity, likely through increased gene expression [41,43]. This increased activity results in a higher post-prandial clearance rate of triglyceride-rich lipoproteins. These effects, in turn, may have an effect on LDL particle size, causing a shift from the more atherogenic small dense LDL to larger less atherogenic LDL particles [44,45]. However, Dunbar et al. showed that the reduction in triglyceride-rich lipoproteins was independent of the accompanying decrease in cholesterol-rich lipoproteins, including LDL [42]. This would suggest, therefore, that EPA-induced increases in LDL clearance occurs via a separate mechanism.