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In India large number of Diabeies are thin (BMI < 19). They manifest with different
presentation, morbidity & mortality patterns as well as biochemical & hormonal profile when compared with classical patients with NIDDM. Some postulate that uncared poorly controlled diabetic state is the causes of leaness is obviated by the fact that they continue to be lean even after years of good metabolic control.
Distribution of Type 2 DM as per BMI 322 patients3
| |
Number |
Percentage |
BMI |
| Obese |
25 |
7-8% |
7.7 > 21 > 25 |
| Non obese |
212 |
65-8 |
20-27 |
| Lean |
85 |
26.4 |
19 & below (17.9%) (B.K. Sahay) |
Incidence of lean NIDDM was observed to be 11 to 25 percent in all diabetics diagnosed as NIDDM in different studies. Leaness is an interesting characteristics of these individuals. Good metabolic control and affluence has little effect on their constitution, natural history and morbidity.
Though initially for some years they may respond to oral sulphonyl urea. These diabetics
in due course more often become insulin requiring as compared to classical NIDDM. They may respond well to combination of sulphonyl urea and insulin (Intermediates).
Age distribution in 89 lean NIDDM2
< 30 - 20.2% 31 - 40 - 25.8% > 40 - 53.9
Clinical Presentation & Morbidity Pattern
Adult patients present with symptoms and signs suggestive of long standing hyperglycaemia. Peripheral neuropathy was the commonest presenting features in the lean while hypertension and CAD were conspicuously absent in lean NIDDM. Microangiopathy was present in 3% of cases at diagnosis. Pulmonary tuberculosis had the highest associatin with these subjects. Suggesting increased susceptibility to infection. Higher incidence of infection, neuropathy and stroke with obvious paucity of CAD and hypertension is the typical natural history of these diabetics. They also get retinopathy and nephropathy. Ketosis resistance in these patients is postulated to be due to impaired ketogenic process and or deficient adipose tissue.
Lean type 2 DM have moderates to severe basal hyperglycaemia. Euglycemia can be
achieved with sulphonylurea at earlier stages of disease. Lean type 2 there was hyper active futile cycles of carbohydrate metabolism in the liver. This metabolic aberration is the reverse of what has been observed in NIDDM of the west. Lean type 2 DM have lower cholesterol, higher HDL cholesterol even in uncontrolled state. Their triglyceride, FFA and lactate levels are higher suggesting excess production by liver. Angiotensin sensitivity is negatively correlated with blood glucose levels.
Hormonal Changes in Lean NIDDM
Serum insulin levels are lower both during fasting and fed state compared to obese and normal weight DM. C-peptide response to glucose was there.
Lean DM also show low normal values of growth hormone at basal state. The lean had a
much higher FBG level than the obese. When they were subjected to B-cell secretagogue like glucose and IV glucagon mere was good response but still IRI levels were persisting lower in the lean at all stages. All these suggest a good B-cell reserve in lean with probably excess extraction of insulin in the porto hepatic circulation leading to lower peripheral levels of insulin.
Conclusion
Lean type 2 DM is probably resulting from under nutrition and its adverse effects on B-cell
function. It has atypical clinical, biochemical and hormonal profile. This type of diabetics are seen about 10-25% in our country.
REFERENCES
1. Kannan K., Lean—Type 2 Diabetes Mellitus—A distinct entity. Page 147-151—-
NNDU 93 proceeding. Edited by : Anil Kapur, Published by Healthcare
Communication.
2. Siddarth Das, Lean NTDDM - An independent entity. Page 153-160 NNDU 93
proceeding. Edited by : Anil Kapur, Published by Healthcare Communication.
3. B. K. Sahay—Profile of Lean NIDDM as seen in Hyderabad. Page 161-164, NNDU
93 proceeding. Edited by Anil Kapur, Published by Health Care Communication.
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