Plasma Level of Glucagon-like Peptide 1 in Obese Egyptians with Normal and Impaired Glucose Tolerance

Hussein, Magda S.; Abushady, Manal; Refaat, Safa; Ibrahim, Rasha Y.M.

doi:10.1016/j.arcmed.2013.10.012

Cited by 25 publications

(18 citation statements)

References 17 publications

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“…For example, our research has shown that HFD decreased some state of oxidative phosphorylation in the frontal cortex and similar changes were found in skeletal muscle of type 2 diabetic patients (Mogensen et al 2007). Moreover, in the current studies, HFD decreased the level of GLP-1 in the frontal cortex and in obese people, and plasma level of this hormone was also lower than in controls (Hussein et al 2014). Similar effect on GLUT1 transporters to that which we observed in the frontal cortex of PS-NR rats fed a HFD was detected in fibroblast and skeletal muscles of obese people (Miele et al 1997).…”

Section: Frontal Cortex Hippocampussupporting

confidence: 84%

Brain Metabolic Alterations in Rats Showing Depression-Like and Obesity Phenotypes

et al. 2019

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Current data suggest an important role of brain metabolic disturbances in the pathogenesis of depression and obesity, diseases that frequently co-occur. Our aim was to determine whether there are changes in markers characterizing glucose metabolism in prenatal stress (PS; animal model of depression), in rats fed a high-fat diet (HFD), and especially in the model of depression and obesity co-occurrence. The changes in glucose-6-phosphate, glycogen, glucose transporters (GLUT1, GLUT4), glucagonlike peptide-1 receptor (GLP-1R), and mitochondrial complexes levels in the frontal cortex and/or hippocampus were observed. In the case of the coexistence of depression and obesity, the most important changes were (1) the decrease in the membrane form of GLUT4, which may suggest weaker insulin action in the frontal cortex, and (2) the diminished GLP-1R, which could cause neurodegenerative changes in the hippocampus. However, presented results suggested that HFD weakened the PS effect of uncoupling oxidative phosphorylation in the frontal cortex.

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Section: Frontal Cortex Hippocampussupporting

confidence: 84%

Brain Metabolic Alterations in Rats Showing Depression-Like and Obesity Phenotypes

et al. 2019

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“…In accordance with the findings discussed above, the overfeeding intervention did not stimulate any changes in fasted or postprandial concentrations of the orexigenic (38) hormone acylated ghrelin or the anorectic (38,39) hormones PYY and GLP-1. These peptides represent key markers of impaired appetite regulation in obese individuals, as depressed concentrations of PYY and GLP-1, and reduced ghrelin responses to feeding are thought to be implicated in reduced satiety and hyperphagia (40)(41)(42)(43) . The findings from the present study support previous evidence that 3-7 days of overfeeding does not induce any changes in circulating ghrelin and GLP-1 concentrations (10,11,14) .…”

Section: Discussionmentioning

confidence: 99%

A single day of mixed-macronutrient overfeeding does not elicit compensatory appetite or energy intake responses but exaggerates postprandial lipaemia during the next day in healthy young men

et al. 2019

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Discrete episodes of overconsumption may induce a positive energy balance and impair metabolic control. However, the effects of an ecologically relevant, single day of balanced macronutrient overfeeding are unknown. Twelve healthy men (of age 22 (sd 2) years, BMI 26·1 (sd 4·2) kg/m2) completed two 28 h, single-blind experimental trials. In a counterbalanced repeated measures design, participants either consumed their calculated daily energy requirements (energy balance trial (EB): 10 755 (sd 593) kJ) or were overfed by 50 % (overfeed trial (OF): 16 132 (sd 889) kJ) under laboratory supervision. Participants returned to the laboratory the next day, after an overnight fast, to complete a mixed-meal tolerance test (MTT). Appetite was not different between trials during day 1 (P>0·211) or during the MTT in the fasted or postprandial state (P>0·507). Accordingly, plasma acylated ghrelin, total glucagon-like peptide-1 and total peptide YY concentrations did not differ between trials during the MTT (all P>0·335). Ad libitum energy intake, assessed upon completion of the MTT, did not differ between trials (EB 6081 (sd 2260) kJ; OF 6182 (sd 1960) kJ; P=0·781). Plasma glucose and insulin concentrations were not different between trials (P>0·715). Fasted NEFA concentrations were lower in OF compared with EB (P=0·005), and TAG concentrations increased to a greater extent on OF than on EB during the MTT (P=0·009). The absence of compensatory changes in appetite-related variables after 1 d of mixed macronutrient overfeeding highlights the limited physiological response to defend against excess energy intake. This supports the concept that repeated discrete episodes of overconsumption may promote weight gain, while elevations in postprandial lipaemia may increase CVD risk.

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“…Obesity with the onset of insulin resistance and consequent metabolic diseases, such as impaired glucose tolerance and type 2 diabetes, impairs the effect of incretins. Postprandial GLP-1 concentration in obese people is lower than in people with normal body weight [24][25][26][27]. Similarly, lower postprandial GLP-1 values were measured in patients with type 2 diabetes, while the GIP response in this population was preserved [28][29][30][31][32].…”

Section: Incretin Hormonesmentioning

confidence: 89%

Incretin System: New Pharmacological Target in Obese Women with Polycystic Ovary Syndrome

Sever¹,

Ferjan²

2018

Debatable Topics in PCOS Patients

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Introduction: Obesity is highly prevalent in polycystic ovary syndrome (PCOS). It aggravates adverse features of the syndrome. Weight management by lifestyle intervention is often insufficient. We reviewed studies addressing the use of agents mediating through incretin system in obese PCOS. Material and methods: Available relevant clinical trials were searched from PubMed. Results: Intervention with glucagon-like peptide 1 (GLP-1) analogue liraglutide is associated with consistent body mass index (BMI) reduction in treatment-naive obese women with PCOS and in poor responders to metformin and lifestyle modification. We recognized metformin as a well-suited combination with liraglutide. We demonstrated that liraglutide could also improve eating behavior and fertility potential in obese PCOS. Furthermore, we challenged the potential association of variability of GLP-1 receptor genotype and interindividual differences in response to liraglutide. In addition, we introduced the original concept related to the enhancement of incretin axis through phosphodiesterase 4 (PDE4). Nevertheless, we considered dipeptidyl peptidase 4 inhibitors as an alternative pharmacological intervention in metformin intolerant patients with PCOS. Conclusion: Agents mediating through incretin system in combination with lifestyle intervention and metformin could improve treatment outcomes in obese PCOS patients. Further studies are needed to establish the benefit/risk profile achieved by these potential new treatment strategies.

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Plasma Level of Glucagon-like Peptide 1 in Obese Egyptians with Normal and Impaired Glucose Tolerance

Cited by 25 publications

References 17 publications

Brain Metabolic Alterations in Rats Showing Depression-Like and Obesity Phenotypes

Brain Metabolic Alterations in Rats Showing Depression-Like and Obesity Phenotypes

A single day of mixed-macronutrient overfeeding does not elicit compensatory appetite or energy intake responses but exaggerates postprandial lipaemia during the next day in healthy young men

Incretin System: New Pharmacological Target in Obese Women with Polycystic Ovary Syndrome

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