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 Table of Contents  
Year : 2013  |  Volume : 2  |  Issue : 1  |  Page : 57-58

Lean type diabetes: Changing fads

1 Departments of Internal Medicine; Critical Care, Princess Durru Shehvar Children's and General Hospital, Purani Haveli, Hyderabad, Andhra Pradesh, India
2 Departments of Internal Medicine, Princess Durru Shehvar Children's and General Hospital, Purani Haveli, Hyderabad, Andhra Pradesh, India

Date of Web Publication17-Apr-2013

Correspondence Address:
Dilip Gude
Department of Internal Medicine and Critical Care, Hyderabad 500 001, Andhra Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2278-344X.110569

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How to cite this article:
Gude D, Abbas A. Lean type diabetes: Changing fads. Int J Health Allied Sci 2013;2:57-8

How to cite this URL:
Gude D, Abbas A. Lean type diabetes: Changing fads. Int J Health Allied Sci [serial online] 2013 [cited 2022 May 22];2:57-8. Available from: https://www.ijhas.in/text.asp?2013/2/1/57/110569


Epidemiological profile of type 2 diabetes in India is very different compared to the west. Eighty percent of type 2 diabetic patients in India are non-obese and 1/4 th of type 2 diabetics in India are of Body Mass Index (BMI) <19 kg/m 2 . [1] The build/habitus of these patients is often "lean" with low bodyweight, i.e., more than 20% below the ideal bodyweight for height and gender. The prevalence of lean type diabetes (LTD) with BMI <19 kg/m 2 in India ranges from 1.6% to 26%. [2] They display an atypical clinical, biochemical, and hormonal profile. LTDs tend to be older at diagnosis. The average age distribution in LTDs is believed to be <30 years - 20.2%, 31-40 years - 25.8%, and >40 years - 53.9%. [3] LTDs are distinct variants of classical Type 2 DM (neither Latent Autoimmune Diabetes of Adulthood (LADA) nor former fruste of Type 1 DM).

Leaner patients (BMI <25 kg/m 2 ) compared to obese (BMI ≥30 kg/m 2 ) may have a stronger genetic predisposition (presence of LAMA1 gene, [4] KCNJ15 (potassium inwardly-rectifying channel, subfamily J, member 15), etc.,) to type 2 diabetes. [5] KCNJ15 may be a new pharmacological target (that blocks glucose-stimulated insulin secretion) for individuals with reduced insulin secretion.

LTDs have good insulin C-peptide reserve for a prolonged period of life. LTDs may have excess extraction of insulin in hepatic bed, hyperactive cytochrome system, and non-suppressible glucokinase activity, owing to perturbed insulin kinetics and carbohydrate metabolism. These may result in hypoinsulinemia, hyperglycemia, and dyslipidemia. They have lesser insulin resistance and poorer insulin secretory capacity. Non-insulin-mediated glucose uptakes may be normal but glucose effectiveness-at-zero-insulin (GEZI) may be diminished in insulin-sensitive LTDs. [6] (GEZI = Glucose effectiveness at basal insulin (SG) - (insulin sensitivity index (SI) Χ basal insulin); Concept of GEZI was introduced to eliminate the effect of basal insulin on SG and estimate insulin-independent glucose uptake). [7]

Deterioration in the pancreatic response to glucose stimulus points to profound alteration in carbohydrate metabolism. Undernutrition and poor β-cell function (although markers of autoimmune destruction of β-cells are absent in the majority) may play etiological role in LTDs. Intramyocellular lipid (IMCL) accumulation plays an important role in causing muscle insulin resistance in LTDs, which reverses with modest weight loss. [8] In a study, antibodies to glutamic acid decarboxylase-65 (GAD Ab) were present in 25.3% of LTD. GAD Ab positivity correlated with younger age and lower beta cell function (homeostasis model assessment, HOMA) as compared to the GAD Ab-negative group. [9] Plasma FFA, IL-6, hsCRP, leptin, and triglyceride concentrations are lower in LTDs as opposed to their obese counterparts. [10] Angiotensin sensitivity is negatively correlated with blood glucose levels. LTDs also manifest ketosis resistance owing to impaired ketogenic process and/or deficient adipose tissue. They have moderate to severe basal hyperglycemia with much higher fasting blood glucose level than the obese. Serum insulin level is lower in LTDs than in obese type 2 diabetics, although there is no significant difference in c-peptide level (owing to excess extraction of insulin by the liver). Immunoreactive insulin levels are persistently lower in LTDs both during fasting and fed state compared to obese and normal weight DM with adequate c-peptide response to glucose. Excess extraction of insulin in the porto-hepatic circulation in LTDs leads to lower peripheral levels of insulin. LTDs show low normal values of growth hormone at basal state.

Higher prevalence of microvascular complications (peripheral neuropathy (70%), retinopathy (25%), and nephropathy (13%)) in LTDs are observed compared to diabetics with ideal body weight or obese diabetic patients. [2] These are related to duration of diabetes and glycemic control. Higher incidence of infection (increased rate of pulmonary tuberculosis [3] ) and stroke are more common features in the LTDS while coronary artery disease (CAD) and hypertension are characteristically absent. LTDs have lower cholesterol, higher HDL cholesterol (excess hepatic lipase activity), higher triglyceride, free-fatty acids, and lactate levels. In LTDs, increase in urinary albumin excretion may be an indicator for development of proliferative diabetic retinopathy. [11] The insulin resistance in LTDs is not related to anthropometric parameters like central obesity and waist-hip ratio.

Sulfonylureas and other oral hypoglycemic agents (OHA) benefit LTDs at earlier stages, but eventually they may succumb to secondary OHA failure (observed in about 27%). [2] The presence of insulin resistance and a good beta-cell reserve for insulin, despite lean habitus, enables LTDs responsive to OHA initially.

LTD is an increasingly common entity that might pose diagnostic challenge and warrants prompt awareness by clinicians of its features and management.

  Acknowledgment Top

We thank our colleagues and staff of Internal medicine.

  References Top

1.Das S. Lean type 2 diabetes mellitus: Profile, peculiarities and paradox.In API Textbook of Medicine. 8th ed. vol 18. 2008. p. 94-104. Editor Dr. Siddharth N. Shah published by API, Mumbai.  Back to cited text no. 1
2.Barma PD, Ranabir S, Prasad L, Singh TP. Clinical and biochemical profile of lean type 2 diabetes mellitus. Indian J Endocrinol Metab 2011;15:S40-3.  Back to cited text no. 2
3.Das S, Lean NI. An independent entity. In: Kapur A, editor. Novo Nordisk Diabetes Update Proceedings. Mumbai: Health Care Communications; 1993. p. 153-9.  Back to cited text no. 3
4.Perry JR, Voight BF, Yengo L, Amin N, Dupuis J, Ganser M, et al. Stratifying type 2 diabetes cases by BMI identifies genetic risk variants in LAMA1 and enrichment for risk variants in lean compared to obese cases. PLoS Genet 2012;8:e1002741.  Back to cited text no. 4
5.Okamoto K, Iwasaki N, Nishimura C, Doi K, Noiri E, Nakamura S, et al. Identification of KCNJ15 as a susceptibility gene in Asian patients with type 2 diabetes mellitus. Am J Hum Genet 2010;86:54-64.  Back to cited text no. 5
6.García-Estévez DA, Araújo-Vilar D, Saavedra-González A, Fiestras-Janeiro G, Cabezas-Cerrato J. Glucose metabolism in lean patients with mild type 2 diabetes mellitus: Evidence for insulin-sensitive and insulin-resistant variants. Metabolism 2002;51:1047-52.  Back to cited text no. 6
7.Kahn SE, Prigeon RL, Mc Culloch DK, Boyko EJ, Bergman RN, Schwartz MW, et al. The contribution of insulin-dependent and insulin-independent glucose uptake to intravenous glucose tolerance in healthy human subjects. Diabetes 1994;43:587-92.  Back to cited text no. 7
8.Petersen KF, Dufour S, Morino K, Yoo PS, Cline GW, Shulman GI. Reversal of muscle insulin resistance by weight reduction in young, lean, insulin-resistant offspring of parents with type 2 diabetes. Proc Natl Acad Sci U S A 2012;109:8236-40.  Back to cited text no. 8
9.Unnikrishnan AG, Singh SK, Sanjeevi CB. Prevalence of GAD65 antibodies in lean subjects with type 2 diabetes. Ann N Y Acad Sci 2004;1037:118-21.  Back to cited text no. 9
10.Hansen D, Dendale P, Beelen M, Jonkers RA, Mullens A, Corluy L, et al. Plasma adipokine and inflammatory marker concentrations are altered in obese, as opposed to non-obese, type 2 diabetes patients. Eur J Appl Physiol 2010;109:397-404.  Back to cited text no. 10
11.Singh SK, Behre A, Singh MK. Diabetic retinopathy and microalbuminuria in lean type 2 diabetes mellitus. J Assoc Physicians India 2001;49:439-41.  Back to cited text no. 11

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