Dipeptidyl Peptidase 4 Activity Is Related to Body Composition, Measures of Adiposity, and Insulin Resistance in Subjects with Excessive Adiposity and Different Degrees of Glucose Tolerance

Júnior, Wellington Santana da Silva; Souza, Maria das Graças Coelho de; Neto, José Firmino Nogueira; Kraemer‐Aguiar, Luiz Guilherme

doi:10.1155/2019/5238013

Cited by 11 publications

(13 citation statements)

References 31 publications

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“…GLP-1 and GIP are incretin hormones with welldemonstrated insulinotropic effects (40). In the present study, to minimize the impact of active hormone levels interindividual variability derived from variable dipeptidyl peptidase 4 (DPP4) activity according to individuals' weight and circulating insulin levels (46), total GLP-1 and GIP levels were measured. Subjects that developed postprandial hypoglycemia presented higher postprandial GLP-1 levels, consistent with some (2, 11) but not all previous reports (30).…”

Section: Discussionmentioning

confidence: 99%

A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia

et al. 2020

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Obesity and obesity-related diseases are major public health concerns that have been exponentially growing in the last decades. Bariatric surgery is an effective long-term treatment to achieve weight loss and obesity comorbidity remission. Post-bariatric hypoglycemia (PBH) is a late complication of bariatric surgery most commonly reported after Roux-en-Y gastric bypass (RYGB). PBH is the end result of postprandial hyperinsulinemia but additional endocrine mechanisms involved are still under debate. Our aim was to characterize entero-pancreatic hormone dynamics associated with postprandial hypoglycemia after RYGB. Individuals previously submitted to RYGB (N=23) in a single tertiary hospital presenting PBH symptoms (Sym, n=14) and asymptomatic weight-matched controls (Asy, n=9) were enrolled. Participants underwent a mixed-meal tolerance test (MMTT) to assess glucose, total amino acids (total AA), insulin, C-peptide, glucagon, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and neurotensin (NT). We found that hypoglycemia during the MMTT was equally frequent in Sym and Asy groups (p=1.000). Re-grouped according to glucose nadir during the MMTT (Hypo n=11 vs NoHypo n=12; nadir <3.05 mmol/l vs ≥3.05 mmol/l), subjects presented no differences in anthropometric (BMI: p=0.527) or metabolic features (HbA1c: p=0.358), yet distinct meal-elicited hormone dynamics were identified. Postprandial glucose excursion and peak glucose levels were similar (p>0.05), despite distinct late glycemic outcomes (t=60 min and t=90 min: p<0.01), with overall greater glycemic variability in Hypo group (minimum-to-maximum glucose ratio: p<0.001). Hypo group meal-triggered hormone profile was characterized by lower early glucagon (t=15 min: p<0.01) and higher insulin (t=30 min: p<0.05, t=45 min: p<0.001), C-peptide (t=30 min: p<0.01, t=45 min: p<0.001, t=60 min: p<0.05), and GLP-1 (t=45 min: p<0.05) levels. Hyperinsulinemia was an independent risk factor for hypoglycemia (p<0.05). After adjusting for hyperinsulinemia, early glucagon correlated with glycemic nadir (p<0.01), and prevented postprandial hypoglycemia (p<0.05). A higher insulin to glucagon balance in Hypo was observed (p<0.05). No differences were observed in total AA, GIP or NT excursions (p>0.05). In sum, after RYGB, postprandial hyperinsulinemia is key in triggering PBH, but a parallel and earlier rise in endogenous glucagon might sustain the inter-individual variability in glycemic outcome beyond the effect of hyperinsulinism, advocating a potential pivotal role for glucagon in preventing hyperinsulinemic hypoglycemia.

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Section: Discussionmentioning

confidence: 99%

A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia

et al. 2020

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“…There is a direct association between DPP4 activity and IR in humans [ 143 ], and evidence that obesity in mice stimulates hepatocytes to synthesize and secret DPP4, which acts with plasma factor Xa to promote inflammation of AT macrophages and IR [ 144 ] (Fig. 1 ).…”

Section: Nafld Treatmentmentioning

confidence: 99%

NAFLD as a continuum: from obesity to metabolic syndrome and diabetes

Godoy-Matos

Júnior

Valério

2020

Diabetol Metab Syndr

Self Cite

439

287

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Background: The prevalence of non-alcoholic fatty liver disease (NAFLD) has been increasing rapidly. It is nowadays recognized as the most frequent liver disease, affecting a quarter of global population and regularly coexisting with metabolic disorders such as type 2 diabetes, hypertension, obesity, and cardiovascular disease. In a more simplistic view, NAFLD could be defined as an increase in liver fat content, in the absence of secondary cause of steatosis. In fact, the clinical onset of the disease is a much more complex process, closely related to insulin resistance, limited expandability and dysfunctionality of adipose tissue. A fatty liver is a main driver for a new recognized liver-pancreatic α-cell axis and increased glucagon, contributing to diabetes pathophysiology. Main text: This review will focus on the clinical and pathophysiological connections between NAFLD, insulin resistance and type 2 diabetes. We reviewed non-invasive methods and several scoring systems for estimative of steatosis and fibrosis, proposing a multistep process for NAFLD evaluation. We will also discuss treatment options with a more comprehensive view, focusing on the current available therapies for obesity and/or type 2 diabetes that impact each stage of NAFLD. Conclusion: The proper understanding of NAFLD spectrum-as a continuum from obesity to metabolic syndrome and diabetes-may contribute to the early identification and for establishment of targeted treatment.

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“…The relationship between HbA1c and body composition is controversial in patients with DM. In addition, plasma DPP4 activity is reported to be positively correlated with lean mass and central adiposity, and negatively with general adiposity 45 . Sulfonylurea has the well-known side effects of weight gain 46 , which might lead to change body composition.…”

Section: Discussionmentioning

confidence: 99%

The Association of Targeted Gut Microbiota with Body Composition in Type 2 Diabetes Mellitus

Hung¹,

Hung²,

Tsai³

et al. 2021

Int. J. Med. Sci.

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The association between body composition and gut microbiota in type 2 diabetes mellitus (DM) remains unknown. To elucidate the correlation of body composition and gut microbiota, we conducted a clinical study to enroll 179 patients with type 2 DM. Body composition of lean tissue index (LTI) and fat tissue index was measured by Body Composition Monitor. Eight pairs of 16S rRNA gene primers specific to Firmicutes, Bacteroidetes, the Clostridium leptum group, Bacteroides , Bifidobacterium , Akkermansia muciniphila , Escherichia coli , and Faecalibacterium prausnitzii were used to measure their abundance by quantitative polymerase chain reaction. The results showed that type 2 DM with higher abundance of phylum Firmicutes and a higher ratio of phyla Firmicutes to Bacteroidetes (phyla F/B ratio) had higher LTI. This significant correlation between phyla F/B ratio and LTI was especially evident in type 2 DM with high body mass index, and independent of glycemic control or dipeptidyl peptidase-4 inhibitor usage. In conclusion, our study demonstrated the positive association of LTI with the abundance of phylum Firmicutes and the phyla F/B ratio in type 2 DM.

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Dipeptidyl Peptidase 4 Activity Is Related to Body Composition, Measures of Adiposity, and Insulin Resistance in Subjects with Excessive Adiposity and Different Degrees of Glucose Tolerance

Cited by 11 publications

References 31 publications

A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia

A Potential Role for Endogenous Glucagon in Preventing Post-Bariatric Hypoglycemia

NAFLD as a continuum: from obesity to metabolic syndrome and diabetes

The Association of Targeted Gut Microbiota with Body Composition in Type 2 Diabetes Mellitus

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