PMID- 19896982
OWN - NLM
STAT- MEDLINE
DCOM- 20100223
LR  - 20220408
IS  - 1873-1686 (Electronic)
IS  - 0167-0115 (Linking)
VI  - 159
IP  - 1-3
DP  - 2010 Jan 8
TI  - Fasting plasma levels of nesfatin-1 in patients with type 1 and type 2 diabetes 
      mellitus and the nutrient-related fluctuation of nesfatin-1 level in normal 
      humans.
PG  - 72-7
LID - 10.1016/j.regpep.2009.11.003 [doi]
AB  - The novel satiety factor nesfatin-1 has been shown to decrease food intake and 
      body weight in rodents after i.c.v. injection. However, no further developments 
      regarding the true patho-physiological relevance of nesfatin-1 in obesity and 
      type 1 diabetes mellitus (T1 DM) and type 2 diabetes mellitus (T2 DM) have been 
      reported. A recent study by Stengel et al. demonstrated that a down-regulation of 
      NUCB2 mRNA in gastric endocrine cells was observed after 24-h fasting. They 
      raised the possibility that nesfatin/NUCB2 gene expression may be regulated by 
      nutritional status, suggesting that nesfatin-1 in the stomach might play a role 
      in satiety. In the present study, fasting levels in plasma nesfatin-1, insulin 
      and glucose were measured and analyzed in healthy subjects and in patients with 
      T1 DM and T2 DM. Plasma nesfatin-1 levels were measured 6 times before and after 
      oral glucose ingestion in healthy subjects. No sex differences in plasma 
      nesfatin-1 were found. The mean fasting plasma nesfatin-1 levels were slightly 
      but not significantly higher in T1 DM patients compared to healthy subjects. 
      However, fasting plasma nesfatin-1 levels were significantly lower in T2 DM 
      patients compared to healthy subjects and T1 DM patients. Plasma nesfatin-1 did 
      not change acutely, although a small rise in circulating nesfatin-1 occurred 
      within 30 min after the beginning of an oral glucose ingestion (from a mean basal 
      value of 0.99+/-0.23 ng/ml to a maximum of 1.08+/-0.24 ng/ml). No significant 
      difference in plasma nesfatin-1 before and after an oral glucose was observed. In 
      conclusion, we showed that fasting nesfatin-1 was significantly lower in T2 DM 
      patients compared to healthy subjects and T1 DM patients. The significance of 
      this result is unclear but the reduction in fasting nesfatin-1 may be one of the 
      appetite-related hormones involved in diabetic hyperphagia. In addition, neither 
      glucose nor saline ingestions affected plasma nesfatin-1, suggesting that gastric 
      chemosensation is not sufficient for the nesfatin-1 response under the present 
      conditions.
FAU - Li, Qing-Chun
AU  - Li QC
AD  - Department of Physiology, Qingdao University School of Medicine, Ningxia Road 
      308, Qingdao 266071, China.
FAU - Wang, Hai-Yan
AU  - Wang HY
FAU - Chen, Xi
AU  - Chen X
FAU - Guan, Hong-Zai
AU  - Guan HZ
FAU - Jiang, Zheng-Yao
AU  - Jiang ZY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Regul Pept
JT  - Regulatory peptides
JID - 8100479
RN  - 0 (Calcium-Binding Proteins)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (NUCB2 protein, human)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Nucleobindins)
RN  - 0 (Peptide Hormones)
RN  - 0 (Sweetening Agents)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Administration, Oral
MH  - Adult
MH  - Appetite/drug effects
MH  - Calcium-Binding Proteins
MH  - DNA-Binding Proteins
MH  - Diabetes Mellitus, Type 1/*blood
MH  - Diabetes Mellitus, Type 2/*blood
MH  - Fasting/*blood
MH  - Female
MH  - Food
MH  - Glucose/*administration & dosage
MH  - Humans
MH  - Hyperphagia/blood
MH  - Male
MH  - Middle Aged
MH  - Nerve Tissue Proteins
MH  - Nucleobindins
MH  - Peptide Hormones/*blood
MH  - Sweetening Agents/*administration & dosage
EDAT- 2009/11/10 06:00
MHDA- 2010/02/24 06:00
CRDT- 2009/11/10 06:00
PHST- 2009/05/21 00:00 [received]
PHST- 2009/10/22 00:00 [revised]
PHST- 2009/11/01 00:00 [accepted]
PHST- 2009/11/10 06:00 [entrez]
PHST- 2009/11/10 06:00 [pubmed]
PHST- 2010/02/24 06:00 [medline]
AID - S0167-0115(09)00225-0 [pii]
AID - 10.1016/j.regpep.2009.11.003 [doi]
PST - ppublish
SO  - Regul Pept. 2010 Jan 8;159(1-3):72-7. doi: 10.1016/j.regpep.2009.11.003.