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  • 1
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    The separate and combined impact of the intestinal hormones, GIP, GLP-1, and GLP-2, on glucagon secretion in type 2 diabetes
    American Physiological Society ; 2011
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 300, No. 6 ( 2011-06), p. E1038-E1046
    Details
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 300, No. 6 ( 2011-06), p. E1038-E1046
    Abstract: Type 2 diabetes mellitus (T2DM) is associated with reduced suppression of glucagon during oral glucose tolerance test (OGTT), whereas isoglycemic intravenous glucose infusion (IIGI) results in normal glucagon suppression in these patients. We examined the role of the intestinal hormones glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and glucagon-like peptide-2 (GLP-2) in this discrepancy. Glucagon responses were measured during a 3-h 50-g OGTT ( day A) and an IIGI ( day B) in 10 patients with T2DM [age (mean ± SE), 51 ± 3 yr; body mass index, 33 ± 2 kg/m 2 ; HbA 1c , 6.5 ± 0.2%]. During four additional IIGIs, GIP ( day C), GLP-1 ( day D), GLP-2 ( day E) and a combination of the three ( day F) were infused intravenously. Isoglycemia during all six study days was obtained. As expected, no suppression of glucagon occurred during the initial phase of the OGTT, whereas significantly ( P 〈 0.05) lower plasma levels of glucagon during the first 30 min of the IIGI ( day B) were observed. The glucagon response during the IIGI + GIP + GLP-1 + GLP-2 infusion ( day F) equaled the inappropriate glucagon response to OGTT ( P = not significant). The separate GIP infusion ( day C) elicited significant hypersecretion of glucagon, whereas GLP-1 infusion ( day D) resulted in enhancement of glucagon suppression during IIGI. IIGI + GLP-2 infusion ( day E) resulted in a glucagon response in the midrange between the glucagon responses to OGTT and IIGI. Our results indicate that the intestinal hormones, GIP, GLP-1, and GLP-2, may play a role in the inappropriate glucagon response to orally ingested glucose in T2DM with, especially, GIP, acting to increase glucagon secretion.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    URL: Article
    DOI: 10.1152/ajpendo.00665.2010
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2011
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 603841-4
    SSG: 12
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  • 2
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    Hepatic transcriptome signatures in patients with varying degrees of nonalcoholic fatty liver disease compared with healthy normal-weight individuals
    American Physiological Society ; 2019
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 316, No. 4 ( 2019-04-01), p. G462-G472
    Details
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 316, No. 4 ( 2019-04-01), p. G462-G472
    Abstract: Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of conditions ranging from simple steatosis (NAFL), over nonalcoholic steatohepatitis (NASH) with or without fibrosis, to cirrhosis with end-stage disease. The hepatic molecular events underlying the development of NAFLD and transition to NASH are poorly understood. The present study aimed to determine hepatic transcriptome dynamics in patients with NAFL or NASH compared with healthy normal-weight and obese individuals. RNA sequencing and quantitative histomorphometry of liver fat, inflammation and fibrosis were performed on liver biopsies obtained from healthy normal-weight ( n = 14) and obese ( n = 12) individuals, NAFL ( n = 15) and NASH ( n = 16) patients. Normal-weight and obese subjects showed normal liver histology and comparable gene expression profiles. Liver transcriptome signatures were largely overlapping in NAFL and NASH patients, however, clearly separated from healthy normal-weight and obese controls. Most marked pathway perturbations identified in both NAFL and NASH were associated with markers of lipid metabolism, immunomodulation, extracellular matrix remodeling, and cell cycle control. Interestingly, NASH patients with positive Sonic hedgehog hepatocyte staining showed distinct transcriptome and histomorphometric changes compared with NAFL. In conclusion, application of immunohistochemical markers of hepatocyte injury may serve as a more objective tool for distinguishing NASH from NAFL, facilitating improved resolution of hepatic molecular changes associated with progression of NAFLD. NEW & NOTEWORTHY Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in Western countries. NAFLD is associated with the metabolic syndrome and can progress to the more serious form, nonalcoholic steatohepatitis (NASH), and ultimately lead to irreversible liver damage. Using gold standard molecular and histological techniques, this study demonstrates that the currently used diagnostic tools are problematic for differentiating mild NAFLD from NASH and emphasizes the marked need for developing improved histological markers of NAFLD progression.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    URL: Article
    DOI: 10.1152/ajpgi.00358.2018
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2019
    detail.hit.zdb_id: 1477329-6
    detail.hit.zdb_id: 603840-2
    SSG: 12
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  • 3
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    Glucose-Lowering Effects and Low Risk of Hypoglycemia in Patients With Maturity-Onset Diabetes of the Young When Treated With a GLP-1 Receptor Agonist: A Double-Blind, Randomized, Crossover Trial
    American Diabetes Association ; 2014
    In:  Diabetes Care Vol. 37, No. 7 ( 2014-07-01), p. 1797-1805
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 37, No. 7 ( 2014-07-01), p. 1797-1805
    Abstract: The most common form of maturity-onset diabetes of the young (MODY), hepatocyte nuclear factor 1α (HNF1A diabetes: MODY3) is often treated with sulfonylureas that confer a high risk of hypoglycemia. We evaluated treatment with GLP-1 receptor agonists (GLP-1RAs) in patients with HNF1A diabetes. RESEARCH DESIGN AND METHODS Sixteen patients with HNF1A diabetes (8 women; mean age 39 years [range 23–67 years]; BMI 24.9 ± 0.5 kg/m2 [mean ± SEM] ; fasting plasma glucose [FPG] 9.9 ± 0.9 mmol/L; HbA1c 6.4 ± 0.2% [47 ± 3 mmol/mol] ) received 6 weeks of treatment with a GLP-1RA (liraglutide) and placebo (tablets), as well as a sulfonylurea (glimepiride) and placebo (injections), in randomized order, in a double-blind, crossover trial. Glimepiride was up-titrated once weekly in a treat-to-target manner; liraglutide was up-titrated once weekly to 1.8 mg once daily. At baseline and at the end of each treatment period a standardized liquid meal test was performed, including a 30-min light bicycle test. RESULTS FPG decreased during the treatment periods (−1.6 ± 0.5 mmol/L liraglutide [P = 0.012] and −2.8 ± 0.7 mmol/L glimepiride [P = 0.003] ), with no difference between treatments (P = 0.624). Postprandial plasma glucose (PG) responses (total area under the curve) were lower with both glimepiride (2,136 ± 292 min × mmol/L) and liraglutide (2,624 ± 340 min × mmol/L) compared with baseline (3,127 ± 291 min × mmol/L; P & lt; 0.001, glimepiride; P = 0.017, liraglutide), with no difference between treatments (P = 0.121). Eighteen episodes of hypoglycemia (PG ≤3.9 mmol/L) occurred during glimepiride treatment and one during liraglutide treatment. CONCLUSIONS Six weeks of treatment with glimepiride or liraglutide lowered FPG and postprandial glucose excursions in patients with HNF1A diabetes. The glucose-lowering effect was greater with glimepiride at the expense of a higher risk of exclusively mild hypoglycemia.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc13-3007
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2014
    detail.hit.zdb_id: 1490520-6
    detail.hit.zdb_id: 441231-X
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  • 4
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    Determinants of Fasting Hyperglucagonemia in Patients with Type 2 Diabetes and Nondiabetic Control Subjects
    Mary Ann Liebert Inc ; 2018
    In:  Metabolic Syndrome and Related Disorders Vol. 16, No. 10 ( 2018-12), p. 530-536
    Details
    In: Metabolic Syndrome and Related Disorders, Mary Ann Liebert Inc, Vol. 16, No. 10 ( 2018-12), p. 530-536
    Type of Medium: Online Resource
    ISSN: 1540-4196 , 1557-8518
    URL: Article
    DOI: 10.1089/met.2018.0066
    Language: English
    Publisher: Mary Ann Liebert Inc
    Publication Date: 2018
    detail.hit.zdb_id: 2110505-4
    detail.hit.zdb_id: 2151220-6
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  • 5
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    Therapy for Obesity Based on Gastrointestinal Hormones
    JCFCorp SG PTE LTD ; 2011
    In:  The Review of Diabetic Studies Vol. 8, No. 3 ( 2011), p. 339-347
    Details
    In: The Review of Diabetic Studies, JCFCorp SG PTE LTD, Vol. 8, No. 3 ( 2011), p. 339-347
    Type of Medium: Online Resource
    ISSN: 1613-6071 , 1614-0575
    URL: Article
    DOI: 10.1900/RDS.2011.8.339
    Language: English
    Publisher: JCFCorp SG PTE LTD
    Publication Date: 2011
    detail.hit.zdb_id: 2161490-8
    detail.hit.zdb_id: 2168938-6
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  • 6
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    Glucagon Resistance at the Level of Amino Acid Turnover and Ureagenesis in Obese Subjects with Hepatic Steatosis
    American Diabetes Association ; 2018
    In:  Diabetes Vol. 67, No. Supplement_1 ( 2018-07-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 67, No. Supplement_1 ( 2018-07-01)
    Abstract: Hyperglucagonemia is considered an important pathophysiological trait of type 2 diabetes and occurs also in individuals with obesity. The underlying mechanisms remain unclear. We hypothesized that hyperglucagonemia is a consequence of steatosis-induced glucagon resistance. We examined 15 healthy (BMI: 23.2±1.6 (mean±SD) kg/m2, age 40.9±12.8 years, hepatic steatosis 2:15) and 15 obese individuals (BMI: 33.6±2.1 kg/m2, age 35.8±9.4 years, hepatic steatosis 14:15) in a pancreatic somatostatin clamp with basal insulin (1 mU/kg/h) and low and high glucagon infusion rates (0.6 and 3.0 ng/kg/min). Glucagon sensitivity was assessed as changes in plasma amino acids (AA) and endogenous glucose production (EGP) and urea synthesis (U.S.) measured by tracer techniques. Basal glucagon and AA were significantly higher in obese compared to lean individuals, but no differences in basal EGP or U.S. were observed. In the lean group AA significantly dropped in response to glucagon infusion (p & lt;0,001) whereas no response was observed in the obese group. Accordingly, both glucagon infusion rates resulted in significantly greater EGP and U.S, respectively, in lean vs. obese individuals. In conclusion, our results point to steatosis-induced hepatic glucagon resistance and compensatory glucagon secretion mediated by glucagonotropic amino acids as a likely explanation of obesity-associated hyperglucagonemia. Disclosure M.P. Suppli: None. J.I. Bagger: None. A.B. Lund: Other Relationship; Self; Novo Nordisk A/S. N.J. Wewer Albrechtsen: Speaker's Bureau; Self; Merck Sharp & Dohme Corp.. Other Relationship; Self; Mercodia, Alpco. J.J. Holst: Advisory Panel; Self; Novo Nordisk A/S. Board Member; Self; Zealand Pharma A/S. Speaker's Bureau; Self; Merck Sharp & Dohme Corp., AstraZeneca. Research Support; Self; Danish Diabetes Academy, Novo Nordisk Foundation. Other Relationship; Self; Antag Therapeutics. Other Relationship; Spouse/Partner; Antag Therapeutics. T. Vilsbøll: Advisory Panel; Self; Amgen Inc., Boehringer Ingelheim GmbH, Eli Lilly and Company, AstraZeneca, MSD K.K., Sanofi, Novo Nordisk A/S. Consultant; Self; Amgen Inc., Boehringer Ingelheim GmbH, Eli Lilly and Company, AstraZeneca, MSD K.K., Sanofi, Novo Nordisk A/S. Speaker's Bureau; Self; Amgen Inc., Boehringer Ingelheim GmbH, Eli Lilly and Company, AstraZeneca, MSD K.K., Sanofi, Novo Nordisk A/S. Research Support; Self; Eli Lilly and Company, Novo Nordisk A/S. F.K. Knop: Advisory Panel; Self; AstraZeneca. Consultant; Self; AstraZeneca. Research Support; Self; AstraZeneca. Speaker's Bureau; Self; AstraZeneca. Advisory Panel; Self; Eli Lilly and Company. Speaker's Bureau; Self; Eli Lilly and Company. Advisory Panel; Self; Amgen Inc.. Speaker's Bureau; Self; Merck Sharp & Dohme Corp.. Advisory Panel; Self; Novo Nordisk A/S. Consultant; Self; Novo Nordisk A/S. Speaker's Bureau; Self; Novo Nordisk A/S. Consultant; Self; Amgen Inc.. Advisory Panel; Self; MedImmune, Sanofi. Consultant; Self; Sanofi. Research Support; Self; Sanofi. Speaker's Bureau; Self; Sanofi.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db18-147-OR
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2018
    detail.hit.zdb_id: 80085-5
    detail.hit.zdb_id: 1501252-9
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  • 7
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    Long-acting amylin analogues for the management of obesity
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Current Opinion in Endocrinology, Diabetes & Obesity Vol. 29, No. 2 ( 2022-04), p. 183-190
    Details
    In: Current Opinion in Endocrinology, Diabetes & Obesity, Ovid Technologies (Wolters Kluwer Health), Vol. 29, No. 2 ( 2022-04), p. 183-190
    Abstract: To summarize recent developments of long-acting amylin analogues for the treatment of obesity and to outline their mode of action. Recent findings Amylin is a pancreatic hormone acting to control energy homeostasis and body weight. Activity at the calcitonin and amylin receptors in the area postrema seems to – at least partly – be responsible for these effects of amylin. Both preclinical and early-stage clinical studies investigating long-acting amylin receptor analogues demonstrate beneficial effects on body weight in obesity. Cagrilintide, a novel amylin analogue suitable for once-weekly administration, is in phase II clinical development and has shown promising body weight reducing effects alone and in combination with the glucagon-like peptide 1 receptor agonist semaglutide. Summary Long-acting amylin analogues have emerged as a possible pharmacotherapy against obesity, but more studies are needed to support the utility and long-term effects of this strategy in relevant populations.
    Type of Medium: Online Resource
    ISSN: 1752-296X , 1752-2978
    URL: Article
    DOI: 10.1097/MED.0000000000000716
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2272017-0
    detail.hit.zdb_id: 2273420-X
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  • 8
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    Circulating Levels of the Soluble Receptor for AGE (sRAGE) during Escalating Oral Glucose Dosages and Corresponding Isoglycaemic i.v. Glucose Infusions in Individuals with and without Type 2 Diabetes
    MDPI AG ; 2020
    In:  Nutrients Vol. 12, No. 10 ( 2020-09-24), p. 2928-
    Details
    In: Nutrients, MDPI AG, Vol. 12, No. 10 ( 2020-09-24), p. 2928-
    Abstract: Postprandial glucose excursions are postulated to increase the risk for diabetes complications via the production of advanced glycation end products (AGEs). The soluble receptor of AGEs (sRAGE) likely acts as a decoy receptor, mopping up AGEs, diminishing their capacity for pro-inflammatory and pro-apoptotic signaling. Recent evidence suggests that AGEs and soluble receptor for AGEs (sRAGE) may be altered under postprandial and fasting conditions. Here, we investigated the effects of increasing oral glucose loads during oral glucose tolerance tests (OGTT) and matched isoglycaemic intravenous (i.v.) glucose infusions (IIGI) on circulating concentrations of sRAGE. Samples from eight individuals with type 2 diabetes and eight age-, gender-, and body mass index (BMI)-matched controls, all of whom underwent three differently dosed OGTTs (25 g, 75 g, and 125 g), and three matched IIGIs were utilised (NCT00529048). Serum concentrations of sRAGE were measured over 240 min during each test. For individuals with diabetes, sRAGE area under the curve (AUC0–240min) declined with increasing i.v. glucose dosages (p 〈 0.0001 for trend) and was lower during IIGI compared to OGTT at the 125 g dosage (p = 0.004). In control subjects, sRAGE AUC0–240min was only lower during IIGI compared to OGTT at the 25 g dose (p = 0.0015). sRAGE AUC0–240min was negatively correlated to AUC0–240min for the incretin hormone glucagon-like peptide −1 (GLP-1) during the 75 g OGTT and matched IIGI, but only in individuals with type 2 diabetes. These data suggest that gastrointestinal factors may play a role in regulating sRAGE concentrations during postprandial glucose excursions, thus warranting further investigation.
    Type of Medium: Online Resource
    ISSN: 2072-6643
    URL: Article
    DOI: 10.3390/nu12102928
    Language: English
    Publisher: MDPI AG
    Publication Date: 2020
    detail.hit.zdb_id: 2518386-2
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  • 9
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    DataSheet1.pdf
    Frontiers Media SA ; 2022
    In:  Frontiers in Physiology Vol. 13 ( 2022-9-6)
    Details
    In: Frontiers in Physiology, Frontiers Media SA, Vol. 13 ( 2022-9-6)
    Abstract: Type 2 diabetes (T2D) is a pathophysiology that is characterized by insulin resistance, beta- and alpha-cell dysfunction. Mathematical models of various glucose challenge experiments have been developed to quantify the contribution of insulin and beta-cell dysfunction to the pathophysiology of T2D. There is a need for effective extended models that also capture the impact of alpha-cell dysregulation on T2D. In this paper a delay differential equation-based model is developed to describe the coupled glucose-insulin-glucagon dynamics in the isoglycemic intravenous glucose infusion (IIGI) experiment. As the glucose profile in IIGI is tailored to match that of a corresponding oral glucose tolerance test (OGTT), it provides a perfect method for studying hormone responses that are in the normal physiological domain and without the confounding effect of incretins and other gut mediated factors. The model was fit to IIGI data from individuals with and without T2D. Parameters related to glucagon action, suppression, and secretion as well as measures of insulin sensitivity, and glucose stimulated response were determined simultaneously. Significant impairment in glucose dependent glucagon suppression was observed in patients with T2D (duration of T2D: 8 (6–36) months) relative to weight matched control subjects (CS) without diabetes (k 1 (mM) −1 : 0.16 ± 0.015 (T2D, n = 7); 0.26 ± 0.047 (CS, n = 7)). Insulin action was significantly lower in patients with T2D (a 1 (10 pM min) −1 : 0.000084 ± 0.0000075 (T2D); 0.00052 ± 0.00015 (CS)) and the Hill coefficient in the equation for glucose dependent insulin response was found to be significantly different in T2D patients relative to CS (h: 1.4 ± 0.15; 1.9 ± 0.14). Trends in parameters with respect to fasting plasma glucose, HbA1c and 2-h glucose values are also presented. Significantly, a negative linear relationship is observed between the glucagon suppression parameter, k 1 , and the three markers for diabetes and is thus indicative of the role of glucagon in exacerbating the pathophysiology of diabetes (Spearman Rank Correlation: ( n = 12; (−0.79, 0.002), (−0.73,.007), (−0.86,.0003)) respectively).
    Type of Medium: Online Resource
    ISSN: 1664-042X
    URL: Article
    URL: Article
    DOI: 10.3389/fphys.2022.911616
    DOI: 10.3389/fphys.2022.911616.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2564217-0
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  • 10
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    No effect of the turmeric root phenol curcumin on prednisolone-induced glucometabolic perturbations in men with overweight or obesity
    Bioscientifica ; 2023
    In:  Endocrine Connections Vol. 12, No. 4 ( 2023-04-01)
    Details
    In: Endocrine Connections, Bioscientifica, Vol. 12, No. 4 ( 2023-04-01)
    Abstract: Preclinically, curcumin has been shown to protect against glucocorticoid-induced insulin resistance. We evaluated the effect of curcumin administered with prednisolone in healthy overweight or obese men. Methods In a double-blind, parallel-group trial, 24 overweight/obese non-diabetic men were randomised to one of three intervention groups (A) prednisolone placebo+curcumin placebo, (B) prednisolone (50 mg/day)+curcumin placebo or (C) prednisolone and curcumin (400 mg/day). Curcumin or curcumin placebo treatment started 1 day prior to 10-day prednisolone or prednisolone placebo treatment. The primary endpoint was change in prednisolone-induced insulin resistance assessed by homeostatic model assessment of insulin resistance (HOMA2-IR). Other endpoints included anthropometric measurements, magnetic resonance spectroscopy-assessed hepatic fat content, blood pressure, circulating metabolic markers and continuous glucose monitoring measures. Results Baseline characteristics (mean ± s.d ): age 44.2 ± 13.7 years, BMI 30.1 ± 3.5 kg/m 2 , HbAlc 33.3 ± 3.2 mmol/mol, HOMA2-IR 1.10 ± 0.45 and fasting plasma glucose 5.2 ± 0.4 mmol/L. Prednisolone significantly increased HOMA2-IR (estimated treatment difference 0.36 (95% CI 0.16; 0.57)). Co-treatment with curcumin had no effect on HOMA2-IR (estimated treatment difference 0.08 (95% CI −0.13; 0.39)). Prednisolone increased HbAlc, insulin, C-peptide, glucagon, blood pressure, mean interstitial glucose, time spent in hyperglycaemia and glucose variability, but no protective effect of curcumin on any of these measures was observed. Conclusions In this double-blind, placebo-controlled parallel-group study involving 24 overweight or obese men randomised to one of three treatment arms, curcumin treatment had no protective effect on prednisolone-induced insulin resistance or other glucometabolic perturbations.
    Type of Medium: Online Resource
    ISSN: 2049-3614
    URL: Article
    DOI: 10.1530/EC-22-0334
    Language: Unknown
    Publisher: Bioscientifica
    Publication Date: 2023
    detail.hit.zdb_id: 2668428-7
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