Effects of miglitol, sitagliptin, and initial combination therapy with both on plasma incretin responses to a mixed meal and visceral fat in over-weight Japanese patients with type 2 diabetes. “The MASTER randomized, controlled trial”

Mikada, Atsushi; Narita, Takuma; Yokoyama, Hiroyuki; Yamashita, Risa; Horikawa, Yohei; Tsukiyama, Katsushi; Yamada, Yoshio

doi:10.1016/j.diabres.2014.09.040

Cited by 23 publications

(38 citation statements)

References 41 publications

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“…On the other hand, although adiponectin is known to promote insulin sensitivity, new studies showed the paradoxical association between high serum adiponectin levels and increased cardiovascular mortality rate, suggesting an unexpected deleterious role of adiponectin on atherosclerotic processes in T2DM . Similarly, while we could not demonstrate the effect of metformin on visceral fat (VF), recent studies suggest than other antidiabetic agents, such as ipraglifrozin alone or miglitol combined with sitagliptin , may be more potent in the reduction of VF.…”

Section: Changes In Adiponectin Level and Fat Distribution In Patientcontrasting

confidence: 85%

Research update for articles published in EJCI in 2014

Arellano-Orden

Bacopoulou

Băicuș

et al. 2016

Eur J Clin Investigation

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Section: Changes In Adiponectin Level and Fat Distribution In Patientcontrasting

confidence: 85%

Research update for articles published in EJCI in 2014

Arellano-Orden

Bacopoulou

Băicuș

et al. 2016

Eur J Clin Investigation

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“…Further, BMI contributed 13.0 and 20.8 % to variance in circulating levels of fasting and peak postprandial oxyntomodulin in individuals with NODAP, respectively (i. e., about 2 times more compared with healthy controls). Although evidence shows that GIP is associated with fat accumulation [34], studies conducted until now have largely been limited to either investigations of general and abdominal adiposity (as determined by waist circumference or BMI [35,36]) or a particular fat depot (e. g., liver fat [37]). The present study is the first study to investigate the associations between gut hormones and a comprehensive panel of body fat parameters (▶table 1), on the basis of which it can be inferred that higher liver fat %, and not pancreatic fat %, BMI, SFV, or VFV, appears to be associated with increased GIP levels in individuals with NODAP.…”

Section: Associations Between Gut Hormones and Indices Of Insulin Secmentioning

confidence: 99%

Gut Hormone Responses to Mixed Meal Test in New-Onset Prediabetes/Diabetes After Acute Pancreatitis

et al. 2018

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The study was aimed to investigate gut hormone responses to mixed meal test in individuals with new-onset prediabetes or diabetes after acute pancreatitis (cases) compared with healthy controls, and the effect of body fat parameters. A total of 29 cases and 29 age- and sex-matched healthy controls were recruited. All participants were given standard mixed meal drink and blood samples were collected to measure dipeptidyl peptidase IV, gastric inhibitory peptide, glucagon like peptide-1, insulin, oxyntomodulin, and peptide YY. Body fat parameters were measured using magnetic resonance imaging. Repeated measures and linear regression analyses were conducted in unadjusted and adjusted models. Gastric inhibitory peptide levels were significantly higher whereas oxyntomodulin levels were significantly lower in cases compared with controls in both the unadjusted (p<0.001 and p<0.001, respectively) and adjusted (p<0.001 and p<0.001, respectively) models. In cases, liver fat % contributed up to 13.4% (vs. 2.9% in controls) to variance in circulating levels of gastric inhibitory peptide whereas body mass index - up to 20.8% (vs. 9.9% in controls) in circulating levels of oxyntomodulin. New-onset prediabetes/diabetes after acute pancreatitis is characterised by increased levels of gastric inhibitory peptide and decreased levels of oxyntomodulin. Further, liver fat % and body mass index appear to be the body fat parameters that contribute most significantly to gastric inhibitory peptide and oxyntomodulin levels, respectively.

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“…Several studies have demonstrated that DPP-4 inhibitors offer a wide range of cardiovascular benefits by ameliorating risk factors such as high blood pressure, postprandial lipemia, inflammatory markers, oxidative stress, and platelet aggregation [19]. Recently, sitagliptin has shown to significantly reduce visceral adiposity, as measured with bioelectric impedance analysis (BIA) in overweight type 2 diabetes mellitus patients [20]. The combination of sitagliptin and metformin has shown to be safe and effective [21].…”

Section: Introductionmentioning

confidence: 98%

Effect of sitagliptin on epicardial fat thickness in subjects with type 2 diabetes and obesity: a pilot study

Lima-Martínez

Paoli

Rodney³

et al. 2015

Endocrine

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The aim of the study was to assess the effect of sitagliptin addition on the epicardial adipose tissue (EAT) thickness in subjects with type 2 diabetes mellitus inadequately controlled on metformin monotherapy. This was a 24-week interventional pilot study in 26 consecutive type 2 diabetic patients, 14 females and 12 males average age of 43.8 ± 9.0 years, with Hemoglobin A1c (HbA1c) ≥ 7% on metformin monotherapy. Subjects who met the inclusion criteria were added on sitagliptin and started on sitagliptin/metformin combination at the dosage of 50 mg/1000 mg twice daily. EAT and visceral and total body fat were measured, respectively, with echocardiography and bioelectrical impedance analysis at baseline and after 24 weeks of sitagliptin/metformin treatment in each subject. HbA1c and plasma lipids were also measured. EAT decreased significantly from 9.98 ± 2.63 to 8.10 ± 2.11 mm, p = 0.001, accounting for a percentage of reduction (∆%) of -15% after 24 weeks of sitagliptin addition, whereas total body fat percentage, visceral fat, and body mass index (BMI), decreased by 8, 12, and 7%, respectively (p = 0.001 for all). After 6 month, EAT ∆% was significantly correlated with ∆% of visceral fat (r = 0.456; p = 0.01), whereas no correlation with either BMI ∆% (r = 0.292; p = 0.147) or HbA1c ∆% was found. The addition of Sitagliptin produced a significant and rapid reduction of EAT, marker of organ-specific visceral fat, in overweight/obese individuals with type 2 diabetes inadequately controlled on metformin monotherapy. EAT as measured with ultrasound can serve as no invasive and accurate marker of visceral fat changes during pharmaceutical interventions targeting the fat.

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Effects of miglitol, sitagliptin, and initial combination therapy with both on plasma incretin responses to a mixed meal and visceral fat in over-weight Japanese patients with type 2 diabetes. “The MASTER randomized, controlled trial”

Cited by 23 publications

References 41 publications

Research update for articles published in EJCI in 2014

Research update for articles published in EJCI in 2014

Gut Hormone Responses to Mixed Meal Test in New-Onset Prediabetes/Diabetes After Acute Pancreatitis

Effect of sitagliptin on epicardial fat thickness in subjects with type 2 diabetes and obesity: a pilot study

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