ORCID Profile
0000-0003-4969-4771
Current Organisations
University of Adelaide
,
The University of Adelaide Accounting
,
Northern Adelaide Local Health Network
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Publisher: MDPI AG
Date: 06-09-2023
DOI: 10.3390/NU15183889
Publisher: Springer Science and Business Media LLC
Date: 13-07-2023
DOI: 10.1007/S11154-023-09823-3
Abstract: Background and aims : Bariatric surgery is the most effective treatment in in iduals with obesity to achieve remission of type 2 diabetes. Post-bariatric surgery hypoglycaemia occurs frequently, and management remains suboptimal, because of a poor understanding of the underlying pathophysiology. The glucoregulatory hormone responses to nutrients in in iduals with and without post-bariatric surgery hypoglycaemia have not been systematically examined. Materials and methods : The study protocol was prospectively registered with PROSPERO. PubMed, EMBASE, Web of Science and the Cochrane databases were searched for publications between January 1990 and November 2021 using MeSH terms related to post-bariatric surgery hypoglycaemia. Studies were included if they evaluated in iduals with post-bariatric surgery hypoglycaemia and included measurements of plasma glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), insulin, C-peptide and/or glucagon concentrations following an ingested nutrient load. Glycated haemoglobin (HbA 1c ) was also evaluated. A random-effects meta-analysis was performed, and Hedges’ g (standardised mean difference) and 95% confidence intervals were reported for all outcomes where sufficient studies were available. The τ 2 estimate and I 2 statistic were used as tests for heterogeneity and a funnel plot with the Egger regression-based test was used to evaluate for publication bias. Results : From 377 identified publications, 12 were included in the analysis. In all 12 studies, the type of bariatric surgery was Roux-en-Y gastric bypass (RYGB). Comparing in iduals with and without post-bariatric surgery hypoglycaemia following an ingested nutrient load, the standardised mean difference in peak GLP-1 was 0.57 (95% CI, 0.32, 0.82), peak GIP 0.05 (-0.26, 0.36), peak insulin 0.84 (0.44, 1.23), peak C-peptide 0.69 (0.28, 1.1) and peak glucagon 0.05 (-0.26, 0.36). HbA 1c was less in in iduals with hypoglycaemia − 0.40 (-0.67, -0.12). There was no evidence of substantial heterogeneity in any outcome except for peak insulin: τ 2 = 0.2, I 2 = 54.3. No publication bias was evident. Conclusion : Following RYGB, postprandial peak plasma GLP-1, insulin and C-peptide concentrations are greater in in iduals with post-bariatric surgery hypoglycaemia, while HbA 1c is less. These observations support the concept that antagonism of GLP-1 would prove beneficial in the management of in iduals with hypoglycaemia following RYGB. PROSPERO Registration Number: CRD42021287515.
Publisher: Wiley
Date: 17-03-2023
DOI: 10.1111/DOM.15042
Abstract: To evaluate the effect of gastric distension, induced using a gastric ‘barostat’, on the secretion of glucose‐dependent insulinotropic polypeptide (GIP) and glucagon‐like peptide‐1 (GLP‐1) in the presence and absence of small intestinal nutrients in healthy in iduals. Eight healthy participants (two females, six males, mean age 69.3 ± 1.2 years, body mass index 23.5 ± 0.8 kg/m 2 ) were each studied on four occasions when they received an intraduodenal infusion of either (i) 0.9% saline or (ii) glucose delivered at a rate of 3 kcal/min both with, and without, an intragastric balloon with the pressure set to 8 mmHg above the intragastric minimum distending pressure. Following intraduodenal saline or glucose infusion, there was no difference in plasma GLP‐1 with or without gastric distension ( P = 1.00 for both saline and glucose infusions). There was also no difference in plasma GIP with or without gastric distension ( P = 1.00 for saline infusion and P = .99 for glucose infusion). Gastric distension, either alone or during small intestinal glucose exposure, does not stimulate incretin hormone secretion significantly in healthy humans.
Publisher: Hindawi Limited
Date: 04-11-2018
DOI: 10.1155/2018/7384763
Abstract: Background . Hypocalcaemia is increasingly recognized as a complication of denosumab use in Chronic Kidney Disease (CKD) patients with osteoporosis. Despite Therapeutic Goods Administration (TGA) notifications in 2013, we have subsequently encountered several cases of denosumab-induced hypocalcaemia, raising concern about lack of widespread awareness among prescribing practitioners. Aims . We reviewed the morbidity and healthcare intervention needs of CKD patients with hypocalcaemia attributed to denosumab. Methods . A retrospective case series of CKD patients with clinically significant hypocalcaemia after exposure to denosumab, encountered at the tertiary care referral hospital from December 2013 to February 2017, was undertaken. Results . Eight patients (52-85 years of age) with stage 4-5 CKD developed clinically significant hypocalcaemia (corrected calcium 1.45±0.21mmol/L) following denosumab therapy for osteoporosis. Seven of the eight patients required inpatient management with three patients requiring intravenous calcium replacement and cardiac monitoring in a high dependency unit. Our study also identified additional factors that could potentially contribute to hypocalcaemia such as lack of calcium supplementation, use of noncalcium based phosphate binders, absence of or use of lower doses of calcitriol supplementation, low vitamin D levels, concomitant treatment with loop diuretics, history of parathyroidectomy, or presence of acute medical illness. Conclusion . Multiple cases of severe hypocalcaemia in CKD patients following denosumab exposure were encountered after TGA warnings, resulting in considerable morbidity and intensive healthcare interventions in CKD patients. We advocate greater awareness amongst the medical profession, careful consideration before using denosumab in CKD patients, and close follow-up after administration to prevent morbidity.
Publisher: Wiley
Date: 21-03-2022
DOI: 10.1111/BCP.15297
Abstract: The aim of this study was to evaluate the comparative effects of low‐carbohydrate (LC), full‐strength (FS), and low‐alcohol (LA) beer on gastric emptying (GE), ethanol absorption, glycaemia and insulinaemia in health. Eight subjects (four male, four female age: 20.4 ± 0.4 years BMI 22.7 ± 0.4 kg/m 2 ) had concurrent measurements of GE, plasma ethanol, blood glucose and plasma insulin for 180 min on three separate occasions after ingesting 600 mL of (i) FS beer (5.0% w/v, 246 kcal, 19.2 g carbohydrate), (ii) LC beer (4.6% w/v, 180 kcal, 5.4 g carbohydrate) and (iii) LA beer (2.6% w/v, 162 kcal, 17.4 g carbohydrate) labelled with 20 MBq 99mTc‐calcium phytate, in random order. There was no difference in the gastric 50% emptying time (T50) (FS: 89.0 ± 13.5 min vs LC: 79.5 ± 12.9 min vs LA: 74.6 ± 12.4 min P = .39). Plasma ethanol was less after LA than LC ( P .001) and FS ( P .001), with no difference between LC and FS ( P = 1.0). There was an inverse relationship between plasma ethanol at 15 min and GE after LA ( r = −0.87, P .01) and a trend for inverse relationships after LC ( r = −0.67, P = .07) and FS ( r = −0.69, P = .06). The AUC 0–180 min for blood glucose was greater for LA than LC ( P .001), with no difference between LA and FS ( P = .40) or LC and FS ( P = 1.0). In healthy young subjects, GE of FS, LC and LA beer is comparable and a determinant of the plasma ethanol response.
Publisher: The Endocrine Society
Date: 24-05-2022
Abstract: The relationships of gastric emptying (GE) with the glycemic response at 120 minutes, glucagon-like peptide-1 (GLP-1), and insulin secretion following a glucose load in type 2 diabetes (T2D) are uncertain. We evaluated the relationship of plasma glucose, GLP-1, and insulin secretion with GE of a 75-g oral glucose load in T2D. Single-center, cross-sectional, post hoc analysis. Institutional research center. 43 in iduals with T2D age 65.6 ± 1.1 years, hemoglobin A1c 7.2 ± 1.0%, median duration of diabetes 5 years managed by diet and/or metformin. Participants consumed the glucose drink radiolabeled with 99mTc-phytate colloid following an overnight fast. GE (scintigraphy), plasma glucose, GLP-1, insulin, and C-peptide were measured between 0 and 180 minutes. The relationships of the plasma glucose at 120 minutes, plasma GLP-1, and insulin secretion (calculated by Δinsulin0-30/ Δglucose0-30 and ΔC-peptide0-30/Δglucose0-30) with the rate of GE (scintigraphy) were evaluated. There were positive relationships of plasma glucose at 30 minutes (r = 0.56, P & 0.001), 60 minutes (r = 0.57, P & 0.001), and 120 minutes (r = 0.51, P & 0.001) but not at 180 minutes (r = 0.13, P = 0.38), with GE. The 120-minute plasma glucose and GE correlated weakly in multiple regression models adjusting for age, GLP-1, and insulin secretion (P = 0.04 and P = 0.06, respectively). There was no relationship of plasma GLP-1 with GE. Multiple linear regression analysis indicated that there was no significant effect of GE on insulin secretion. In T2D, while insulin secretion is the dominant determinant of the 120-minute plasma glucose, GE also correlates. Given the relevance to interpreting the results of an oral glucose tolerance test, this relationship should be evaluated further. There appears to be no direct effect of GE on either GLP-1 or insulin secretion.
No related grants have been discovered for Ryan Jalleh.