PMID- 31832130
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220411
IS  - 2042-0188 (Print)
IS  - 2042-0196 (Electronic)
IS  - 2042-0188 (Linking)
VI  - 10
DP  - 2019
TI  - Impaired compensatory hyperinsulinemia among nonobese type 2 diabetes patients: a 
      cross-sectional study.
PG  - 2042018819889024
LID - 10.1177/2042018819889024 [doi]
LID - 2042018819889024
AB  - AIMS: Obesity associated prolonged hyperinsulinemia followed by beta-cell failure is 
      well established as the pathology behind type 2 diabetes mellitus (T2DM). 
      However, studies on nonobese T2DM have reported it to be a distinct clinical 
      entity with predominant insulin secretory defect. We, therefore, hypothesized 
      that compensatory hyperinsulinemia in response to weight gain is impaired in 
      nonobese subjects. METHODS: This was a cross-sectional study from a 
      community-based metabolic health screening program. Adiposity parameters 
      including body mass index (BMI), waist circumference (WC), body fat percentage, 
      plasma leptin concentration and metabolic parameters namely fasting insulin, 
      glucose, total cholesterol, and triglycerides were measured in 650 individuals 
      (73% healthy, 62% nonobese with a BMI <25). RESULTS: In contrast to obese T2DM, 
      nonobese T2DM patients did not exhibit significant hyperinsulinemia compared with 
      the nonobese healthy group. Age, sex, and fasting glucose adjusted insulin 
      levels, homeostatic model assessment of insulin resistance (HOMA-IR) and 
      HOMA-beta cell function (HOMA-B) were increased in obese T2DM compared with 
      nonobese T2DM. Although adiposity parameters showed strong correlation with 
      fasting insulin in obese healthy (r = 0.38, 0.38, and 0.42, respectively; all p 
      values < 0.001) and T2DM (r = 0.54, 0.54, and 0.66, respectively; all p < 0.001), 
      only BMI and leptin showed a weak correlation with insulin in the nonobese 
      healthy group (0.13 and 0.13, respectively; all p < 0.05) which were completely 
      lost in the nonobese T2DM. CONCLUSIONS: Compensatory hyperinsulinemia in response 
      to weight gain is impaired in the nonobese population making insulin secretory 
      defect rather than IR the major pathology behind nonobese T2DM.
CI  - (c) The Author(s), 2019.
FAU - Sarkar, Jit
AU  - Sarkar J
AUID- ORCID: 0000-0002-9964-6287
AD  - Division of Cell Biology and Physiology, CSIR-Indian Institute of Chemical 
      Biology, India.
FAU - Maity, Sujay Krishna
AU  - Maity SK
AD  - National Institute of Pharmaceutical Education & Research, Kolkata, India.
FAU - Sen, Abhishek
AU  - Sen A
AD  - Division of Cell Biology and Physiology, CSIR-Indian, Institute of Chemical 
      Biology, Kolkata, India.
FAU - Nargis, Titli
AU  - Nargis T
AD  - Division of Cell Biology and Physiology, CSIR-Indian, Institute of Chemical 
      Biology, Kolkata, India.
FAU - Ray, Dipika
AU  - Ray D
AD  - Division of Cell Biology and Physiology, CSIR-Indian, Institute of Chemical 
      Biology, Kolkata, India.
FAU - Chakrabarti, Partha
AU  - Chakrabarti P
AUID- ORCID: 0000-0001-9502-8695
AD  - Division of Cell Biology and Physiology, CSIR-Indian, Institute of Chemical 
      Biology, 4 Raja SC Mullick Road, Kolkata, 700032, India.
LA  - eng
PT  - Journal Article
DEP - 20191202
PL  - United States
TA  - Ther Adv Endocrinol Metab
JT  - Therapeutic advances in endocrinology and metabolism
JID - 101532143
PMC - PMC6887811
OTO - NOTNLM
OT  - body mass index
OT  - hyperinsulinemia
OT  - leptin
OT  - nonobese
OT  - type 2 diabetes
OT  - beta-cell failure
COIS- Conflict of interest statement: The author(s) declared no potential conflicts of 
      interest with respect to the research, authorship, and/or publication of this 
      article.
EDAT- 2019/12/14 06:00
MHDA- 2019/12/14 06:01
PMCR- 2019/12/02
CRDT- 2019/12/14 06:00
PHST- 2019/07/03 00:00 [received]
PHST- 2019/10/27 00:00 [accepted]
PHST- 2019/12/14 06:00 [entrez]
PHST- 2019/12/14 06:00 [pubmed]
PHST- 2019/12/14 06:01 [medline]
PHST- 2019/12/02 00:00 [pmc-release]
AID - 10.1177_2042018819889024 [pii]
AID - 10.1177/2042018819889024 [doi]
PST - epublish
SO  - Ther Adv Endocrinol Metab. 2019 Dec 2;10:2042018819889024. doi: 
      10.1177/2042018819889024. eCollection 2019.