4.7 Article

Faecal Microbiota Are Related to Insulin Sensitivity and Secretion in Overweight or Obese Adults

Journal

JOURNAL OF CLINICAL MEDICINE
Volume 8, Issue 4, Pages -

Publisher

MDPI
DOI: 10.3390/jcm8040452

Keywords

faecal microbiota; body mass index; percent body fat; insulin secretion; insulin sensitivity; hyperinsulinaemic-euglycaemic clamp

Funding

  1. National Health and Medical Research Council (NHMRC) [1047897]
  2. Monash University (Australian Postgraduate Award scholarships)
  3. National Heart Foundation (NHF) [100864]
  4. NHMRC [1120070]
  5. Mater Research Foundation
  6. National Health and Medical Research Council of Australia [1120070] Funding Source: NHMRC

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Emerging evidence suggests a role for the gut microbiota in glucose metabolism and diabetes. Few studies have examined the associations between the faecal microbiome and insulin sensitivity and secretion using gold-standard methods in high-risk populations prior to diabetes onset. We investigated the relationships between faecal microbiota composition (16S rRNA sequencing) and gold-standard measures of insulin sensitivity (hyperinsulinaemic-euglycaemic clamp) and insulin secretion (intravenous glucose tolerance test) in 38 overweight or obese otherwise healthy individuals. Genus Clostridium was positively associated with insulin sensitivity, and genera Dialister and Phascolarctobacterium were related to both insulin sensitivity and secretion. Insulin sensitivity was associated with a higher abundance of Phascolarctobacterium and lower abundance of Dialister. Those with higher insulin secretion had a higher abundance of Dialister and lower abundance of Bifidobacterium, compared to those with lower insulin secretion. Body mass index (BMI) was positively correlated with Streptococcus abundance whereas Coprococcus abundance was negatively correlated to BMI and percent body fat. These results suggest that faecal microbiota is related to insulin sensitivity and secretion in overweight or obese adults. These correlations are distinct although partially overlapping, suggesting different pathophysiological pathways. Our findings can inform future trials aiming to manipulate gut microbiome to improve insulin sensitivity and secretion and prevent type 2 diabetes.

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