Background: The aim of the present study was to evaluate whether the different duration of type 1 diabetes mellitus influences basal NPY secretion. Design: The NPY concentrations were measured in sixty-eight men with insulin-dependent diabetes mellitus (IDDM) (duration: group 1 (n.21) &#x3c;5 years (range 2-4 years); group 2 (n.24) &#x3e;5 years and &#x3c;10 years (range: 6-9 years); group 3 (n.29) &#x3e;10 years (range: 11-14 years)) and in age matched normal control subjects (n. 30). Results: The NPY levels were significantly lower in group 3 than in group 2 and 1 and in the control group, in group 2 than in group 1 and in the control group and in group 1 than control group. Conclusion: These results support the view that the duration of diabetes may have a modulatory role in the decreased basal NPY secretion observed in diabetics

Anna Araldi

Claudio Giumelli

Lavinia Volpi

Luigi Capretti

Maria Grazia Magotti

Paolo Chiodera

Riccardo Volpi

Roberta Minelli

Simona Cataldo

Teore Ferri

Vittorio Coiro

English

Nature Precedings

 1
NPY Levels In Type 1 Diabetic Men of Different Duration. 
 
Vittorio Coiro1, Riccardo Volpi1, Simona Cataldo2, Maria Grazia Magotti2, Luigi Capretti3, Anna 
Araldi1, Claudio Giumelli1, Teore Ferri4, Roberta Minelli1, Lavinia Volpi1, Paolo Chiodera1, 2. 
 
1Department of Internal Medicine and Biomedical Sciences, University of Parma 
2Endocrine Service, Hospital of Parma 
3Endocrine Unit, Hospital of Codogno 
4Department of Otolaringology, University of Parma 
 
 
Short Title: NPY levels in diabetes mellitus 
Word count: 1543. 
Key Words: NPY, C-peptide, diabetes mellitus 
 
 
Correspondence: 
Vittorio Coiro, MD 
Department of Internal Medicine and Biomedical Sciences, University of Parma 
Via A. Gramsci 14 
I-43126 Parma, Italy 
Phone & Fax: 0035 0521 033296 
e-mail: vittorio.coiro@unipr.it  
 
 
 
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Abstract 
Background: The aim of the present study was to evaluate whether the different duration of type 1 
diabetes mellitus influences basal NPY secretion.  
Design: The NPY concentrations were measured in sixty-eight  men with insulin-dependent 
diabetes mellitus (IDDM) (duration: group 1 (n.21) <5 years (range 2-4 years); group 2 (n.24) >5 
years and <10 years (range: 6-9 years); group 3 (n.29) >10 years (range: 11-14 years)) and in age 
matched normal control subjects (n. 30).  
Results: The NPY levels were significantly lower in group 3 than in group 2 and 1 and in the 
control group, in group 2 than in group 1 and in the control group and in group 1 than control 
group.  
Conclusion: These results support the view that the duration of diabetes may have a modulatory role 
in the decreased basal NPY secretion observed in diabetics.  
 
Introduction 
The metabolic disturbance of diabetes mellitus (DM) might cause adaptive change in the 
hypothalamic regulation of metabolic control. Such changes may involve regulatory peptides, 
which are known to affect food intake and glucoregulation1-3. 
Disturbance of hypothalamic regulatory peptides could be associated with the impairment of 
hormonal activity in diabetes4,5. The identification of local regulatory peptides activity in diabetes 
may therefore help to clarify hypothalamic control mechanisms. NPY is one of the most widely 
spread neuropeptides in the rat brain. Large amount of NPY are present in several hypothalamic 
sites and immunopositive NPY fibers emanating from NPY producing perikarya in the 
hypothalamic arcuate nucleus and brain stem innerve several hypothalamic regions6,7. In addition, 
NPY plays an important role in the neuroendocrine regulation of eating behaviour1-3, 8-13. 
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Disturbances in NPY function has been observed in diabetes mellitus14,15. Altered hypothalamic 
NPY levels may mediate hyperphagia and polydipsia in diabetic rats16,17 and thus disorders of NPY 
activity might exert an important influence on metabolic control in diabetes.  
Previous studies indicated that different duration of insulin dependent diabetes mellitus (IDDM) 
play a role in the control of LH and AVP secretion. In fact diminution in LH and AVP secretory 
patterns appeared to be more evident in patients with time after the onset of IDDM18-20. In light of 
the difference in LH, AVP secretion, we wondered whether a similar difference also concerns NPY 
secretions. For this purpose, NPY circulating concentrations were measured in diabetic men 
affected by IDDM of different duration. The results obtained in these groups were compared with 
those observed in control age-matched normal men. 
 
Subjects and methods 
Fifty-eight insulin-dependent diabetic men, 23 to 46 years, participated in this study. The duration 
of diabetes ranged from 2 to 14 years. Patients were divided into three group of subjects according 
to the duration of their disease (group 1 (n. 21): <5 years, range 2-4 years; group 2 (n. 24): >5 years 
and <10 years, range 6-9 years; group 3 (n. 23): >10 years, range 11-14 years). The mean age ± SE 
was 29.3±1.8 years in subjects of group 1, 31.2±1.4 in subjects of group 2 and 32.6±1.8 in subjects 
of group 3. Thirty normal  men (27 to 37 years of age) with normal body weight and without signs 
of endocrine diseases or family history of diabetes mellitus participated in this study as controls. All 
subjects were informed of the purpose of the study which was performed according to the Helsinki 
II declaration. The Ethical Committee of the University of Parma, rewieved the protocol of the 
study. None of the diabetic and control subjects were affected by major affective disorders as 
determined by the Hamilton Depressive Rating Scale. None of the diabetic patients received any 
drug, except insulin because of diabetes mellitus, for at least 20 days before the experimental days. 
From the onset of their illness, the patients had been treated with insulin and at the time of this 
study they were hospitalized for adjustment of insulin therapy. Venous blood samples were drawn 
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at 08.00 after a 12 h overnight fast after optimization of insulin administration, which was similar in 
both groups (dose of short acting and intermediate duration monocomponent insulin given together 
twice daily 31.2 ± 2.0 IU/24h (mean ± SE) (group 1), 30.4 ± 1.9 IU/24 h (group 2), 32.0 ± 1.9 
IU/24h group 3. Insulin therapy did not change because the subjects had achieved a good control of 
their metabolic status [average blood glucose: 7.9 ± 0.8 nmol/l (mean ± SE) (group 1), 7.8 ± 0.6 
(group 2), 7.7 ± 0.6 group 3; percent of glycosilated haemoglobin (HbA1c): 7.0 ± 0.8 (mean ± SE) 
(group 1), 7.3 ± 0.7  (group 2), 7.4 ± 0.6 group 3]. No patient had clinical or laboratory evidence of 
ketosis or of associated endocrine or other intercurrent diseases. No signs of autonomic or somatic 
nerve dysfunction or vascular disease were present in any patients. In all of them creatinine 
clearance was in the normal range of values (96.4 ± 4.3 ml/min (mean ± SE) (group 1), 96.2 ± 3.9 
(group 2) 97.6 ± 21.0 group 3; microalbuminuria was absent in all subjects. The mean (± SE) blood 
pressure was 96.5 ± 1.1 mmHg (group 1), 98.1 ± 1.4 mmHg (group 2), 97.8 ±  1.3 (group 3), 97.1 ± 
1.4 mmHg (controls).  All patients underwent ophthalmologic examination to detect the presence of 
diabetic retinopathy. 
Diagnostic criteria. After papillary dilatation patients underwent ophthalmoscopic examination 
performed by the same experienced opthalmologist. The finding of at least three microaneurysms 
was considered a sign of retinopathy. Patients with retinopathy were excluded from the study. As 
control indices of the metabolic status of these patients, blood glucose levels were measured at 7.30 
AM, 11.00 AM and 05.00 PM on the day preceding this experimental study. For each patient, a 
mean value of blood glucose was obtained by averaging these three determinations. On the 
experimental day, blood samples were taken for evaluation of glycaemia and HbA1c. 
Blood glucose concentrations were measured with a glucose oxidase-peroxidase procedure, using 
an IL 918 autoanalyzer (Instrumentation Laboratory, Milan, Italy). HbA1c was measured with 
reagents obtained from Bio-Rad Laboratories (CA, USA). In our laboratory the normal range of 
values for HbA1c is 4.1-6.5%. Plasma NPY levels were measured by RIA utilizing commercial 
kits. The intra-assay and inter-assay coefficients of variation were: 3.6% and 11.0%, respectively. 
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The sensitivity of the method was 6 pmol/l.  Results were analyzed statistically with non-parametric 
Mann-Whitney U test, and linear correlation coefficient of variation as appropriate. All data are 
reported as mean ± SE. 
 
Results 
Clinical and biochemical characteristics of diabetic patients and normal controls are shown in Table 
1.  
Plasma NPY levels were significantly lower in group 2 than in group 1 (P<0.01) and normal 
controls (P<0.01). In group 1 NPY concentrations were lower than in normal controls (P<0.01) 
(Fig. 1). When data obtained in patients of group 1, group 2 and group 3 were combined, significant 
negative correlations were found between duration of diabetes mellitus and NPY concentrations 
(r=0.720; P<0.01). 
 
Discussion 
Our data suggest that changes in plasma NPY levels in diabetics are influenced by the duration of 
the diabetic condition. On the other hand, our patients were in similar metabolic status at the 
moment of the study; and thus the alteration in NPY concentrations cannot be attributed to the 
intercurrent factors such as decreased body weight, poor nutritional conditions or chronic organic 
disorders. More likely the abnormal NPY levels depended on the diabetic conditions per se. A 
limitation of the present study is the measurement of a single fasting hormone concentration. 
However, fasting NPY concentrations is a representative sample of baseline conditions, without the 
influences of pre-prandial or post-prandial factors because NPY concentrations may be influenced 
by food intake. In fact, the evaluation of fasting hormone level is usually a reference point to 
compare two or more populations under different conditions. Because of these reasons, we decided 
to evaluate NPY levels in fasting conditions.  
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The source of circulating NPY concentration remains unclear. NPY is mainly reported to be present 
in the hypothalamic sites including paraventricular and arcuate nucleus21. The blood brain barrier 
(BBB) inhibits the release of peptides into the circulation from various structures in the brain; 
however the arcuate nucleus is known to be a region where the BBB is absent22. Therefore, the 
secretion of NPY from this structure into the blood stream is possible.  
NPY as been also found in the autonomic sympathetic nerve. A recent study reported a mouse 
model which over-expression NPY exclusively in the noradrenergic neurons to evaluate its 
systemic actions when expressed outside of the hypothalamus and the BBB23. In fact, although they 
described an increase of NPY within sympathetic neurons, its blood concentrations was not altered 
in rats. Therefore it is unlikely that autonomic sympathetic neurons are a source of circulating NPY. 
The progressive decline of NPY levels with long-term IDDM might be explained by diabetes-
related alteration of the NPY cell but also it is possible that an unstable glycemic control lasting for 
a long time produced neuroendocrine damages due to relative insulin deficiency; these alterations 
were not reversed by 3 days of continuous insulin infusion before the experiments. Previous reports 
showed decreased concentrations of plasma NPY in subjects with type 1 diabetes mellitus24. In 
contrast, it has been showed an elevation of NPY in type 2 diabetes mellitus patients25,26. In 
diabetics, this suggests that differences in the metabolic status of diabetics might affect the 
circulating concentrations of NPY. As to how relative insulin deficiency may produce NPY 
alterations14 and the site of this action are still unknown. 
A question rising by our data concerns the consequences of the decreased  NPY secretion. Injection 
of NPY is known to stimulate appetite27,28. Therefore the change in ingestive behaviour in diabetes 
mellitus may be attributed to an altered release of NPY.  
The activity of NPYergic neurons in the hypothalamic centers involved in these functions may be 
responsible for the multitude of effects on reproductive, feeding and sexual behaviour in diabetic 
subjects27,28. Our data suggest that NPYergic activity is strongly related with time after the onset of 
IDDM. Further studies are needed to substantiate these hypotheses. 
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behavior in rats. Endocrinology 1985; 117: 2435-2442. 
 
 
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Legend to the Fig. 1 
Basal NPY levels (mean ± SE) in normal controls and in Group 1 and in Group 2 of patients with 
diabetes mellitus. 
 
 
 
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35 
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Normal Controls Group 1 Group 2 
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p < 0.01 
p < 0.02 
p < 0.05 
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Table 1 Clinical and biochemical data of the diabetic men (groups 2 and 3) and normal controls 
_______________________________________________________________________________________________________________________ 
 
   Age (years)  Weight (kg)  BMI  Duration of IDDM  Blood glucose   HbA1c 
(mmol/L-1)   (%) 
 
Group 1 
(n= 21)  29.3±1.8  65.4±1.4  22.0±0.5 <5 (2-4 years)   7.9±0.8   7.0±0.8 
 
Group 2 
(n= 23)  31.2±1.4  64.8±1.7  22.6±0.6 >5 and <10 (6-9 years) 7.8±0.6   7.3±0.7 
 
Control group 
(n= 30)  32.7±1.6  67.4±1.8  23.4±0.4     4.7±0.2   5.6±0.3 
 
_______________________________________________________________________________________________________________________ 
 
 
BMI = Body mass index 
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An arcuatoparaventricular and -dorsomedial hypothalamic neuropeptide Y-containing system which lacks noradrenaline in the rat. Brain Res

Brain monoamines and peptides: role in the control of eating behavior. Fed Proc.

CNS peptides and glucoregulation. Annu Rev Physiol.

Distribution of NPY receptors in the hypothalamus. Neuropeptides

Dopaminergic and cholinergic control of arginine-vasopressin secretion in type 1 diabetic men.

Effect of neuropeptide Y on ingestive behaviors in the rat.

Effect of streptozotocin diabetes on the hypothalamicpituitary-thyroid axis in the rat. Endocrinology

Glucoregulatory effects of intrahypothalamic injections of bombesin and other peptides. Endocrinology

Increased hypothalamic neuropeptide Y concentrations in diabetic rat. Diabetes

Influence of streptozotocin-induced diabetes on growth hormone secretion in the rat. Neuroendocrinology

Interacting appetite-regulating pathways in the hypothalamic regulation of body weight. Endocr Rev

Involvement of neuropeptide Y in neuroendocrine stress responses. Central and peripheral studies. J Neural Transm Suppl.

Large changes in food intake in diabetic rats fed highfat and low-fat diets. Brain Res Bull

Luteinizing hormone response to gonadotropin-releasing hormone and naloxone in menstruating women with type 1 diabetes of different duration. Fert Ster

Metabolic effects of neuropeptide Y injections into the paraventricular nucleus of the hypothalamus. Brain Res

Neuropeptide Y and human pancreatic polypeptide stimulate feeding behavior in rats. Endocrinology

Neuropeptide Y potentiates excitation of supraoptic neurosecretory cells by noradrenaline. Brain Res

Neuropeptide Y stimulates feeding but inhibits sexual behavior in rats. Endocrinology 1985; 117: 2435-2442. N a t u r e P r e c e d i n g s : h d l : / n p r e .

Neuropeptide Y: anatomical distribution and possible function in mammalian nervous system. Life Sci.

Neuropeptide-Y concentration in microdissected hypothalamic regions and in vitro release from the medial basal hypothalamus-preoptic area of streptozotocin-diabetic rats with and without insulin substitution therapy. Endocrinology

Peptide analogue studies of the hypothalamic neuropeptide Y receptor mediating pituitary adrenocorticotrophic hormone release. Proc Natl Acad Sci USA.

Physiologically significant effect of neuropeptide Y to suppress growth hormone release by stimulating somatostatin discharge. Endocrinology 1990; 126: 2296-2301. N a t u r e P r e c e d i n g s : h d l :

Plasma neuropeptide Y (NPY) and galanin before and during exercise in type 1 diabetic patients with autonomic dysfunction. Diabetes Res Clin Pract

Plasma neuropeptide Y differ in distinct diabetic conditions. Neuropeptides

The response of regulatory peptides to moderate hypoglycaemia of short duration in type 1 (insulin-dependent)( diabetes mellitus and in normal man. Diabetes Res

Transgenic mice overexpressing neuropeptide Y in noradrenergic neurons: a novel model of increased adiposity and impaired glucose tolerance. Diabetes

NPY Levels In Type 1 Diabetic Men of Different Duration.

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NPY Levels In Type 1 Diabetic Men of Different Duration.

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