PANCREAS ALERTS
JOP. J
Pancreas (Online) 2012 Jul 10; 13(4):464-469.
Pancreas 2012; Jun 20.
(PMID: 22722259)
Attenuation of acute pancreatitis by
peroxisome proliferator-activated receptor-α in rats: the effect on
toll-like receptor signaling pathways
Ding JL, Zhou ZG, Zhou XY, Zhou B, Wang L, Wang R, et al.
Institute of Digestive Surgery, State Key Laboratory of
Biotherapy, Sichuan University. Sichuan, PR of China
OBJECTIVES: The peroxisome proliferator-activated receptor-α
(PPAR-α) has attracted considerable attention for its anti-inflammatory
properties; however, Toll-like receptor (TLR) pathways have an essential
proinflammatory role in acute pancreatitis (AP). This study aimed to evaluate
the attenuation of inflammation by PPAR-α and to investigate the
interaction between PPAR-α and TLR pathways in AP. METHODS: Acute
pancreatitis was induced in rats by administration of cerulein. The PPAR-α
agonist WY14643 and/or antagonist MK886 was administered. The severity of AP
was determined by measuring serum amylase, lipase, Ca, pathological changes,
myeloperoxidase activity, serum levels of interleukin (IL)-6, and intercellular
adhesion molecule-1 (ICAM-1). The TLR2 and TLR4 messenger RNA (mRNA) and
proteins were determined by real-time reverse transcriptase polymerase chain
reaction and Western blotting, respectively. The mRNA expressions of target
molecules of TLR pathways, including IL-6, IL-10, ICAM-1, and tumor necrosis
factor α were also measured. RESULTS: Treatment with WY14643 significantly
decreased amylase, lipase, myeloperoxidase activity, pathological scores, IL-6,
and ICAM-1 levels. The TLR2 and TLR4 mRNA and proteins were markedly decreased
after treatment with WY14643, along with IL-6, ICAM-1, and tumor necrosis
factor α mRNA levels. However, these effects were completely reversed by
the coadministration of MK886. CONCLUSIONS: Activation of PPAR-α played a
protective role in AP, partially mediated by modulation of TLR pathways.
Pancreas 2012; Jun 20.
(PMID: 22722255)
Factors associated with intolerance
after refeeding in mild acute pancreatitis
Francisco M, Valentín F, Cubiella J, Alves MT, García
MJ, Fernández T, Fernández-Seara J
Department of Gastroenterology, Research Support Unit,
Complexo Hospitalario Universitario de Ourense. Ourense, Spain
OBJECTIVES: This study aimed to describe the mode of refeeding, frequency
of intolerance, and related factors in mild acute pancreatitis (AP). METHODS: The
authors included all cases of mild AP between January 2007 and December 2009 in
an observational, descriptive, and retrospective study. The authors analyzed
demographic and etiological data, admission variables, treatment, refeeding
mode, intolerance frequency, and treatment. Intolerance-related variables were
determined using a Cox regression. RESULTS: Two-hundred thirty-two patients
were included (median age, 74.3 years, bedside index for severity in AP score,
1). Oral diet was reintroduced at 3 days (range, 0-11 days) in 90.9% of cases
with a liquid diet. Intolerance to refeeding appeared in 28 patients (12.1%) at
a median time of 1 day (range, 0-14 days). Oral diet was reduced or suspended
in 71.4%; analgesic and antiemetic drugs were required in 64% and 35.7% of
patients, respectively. The variables independently associated with intolerance
to refeeding were choledocholithiasis (hazard ratio (HR), 12.35; 95% confidence
interval (CI), 2.98-51.19; P=0.001), fasting time (HR, 1.33; 95% CI, 1.09-1.63;
P=0.005), refeeding with complete diet (HR, 4.93; 95% CI, 1.66-14.66; P=0.04),
length of symptoms before admission (HR, 1.004; 95% CI, 1.001-1.006; P=0.012),
and metamizole dose (HR, 1.11; 95% CI, 1.02-1.21; P=0.014). CONCLUSIONS:
Intolerance to refeeding is an infrequent event. The authors have identified
several factors independently associated with intolerance.
Biochim Biophys Acta 2012; Jun 17.
(PMID: 22713802)
Proteomic analysis of the soluble and
the lysosomal+mitochondrial fractions from rat pancreas: implications for
cerulein-induced acute pancreatitis
García-Hernández
V, Sánchez-Bernal C, Sarmiento N, Viana RA, Ferreira L, Pérez N, et al.
Department of Biochemistry and Molecular Biology,
University of Salamanca. Salamanca, Spain
Alterations in protein expression within the initiation phase of acute pancreatitis
(AP) might play an important role in the development of this disease, lysosomes
being involved in its pathophysiology. The use of pancreatic subcellular
fractions in proteomic analysis, simplifies protein maps and helps in the
identification of new protein changes and biomarkers characterizing tissue
damage. The present study aims to determine the differentially expressed acidic
proteins in the pancreatic soluble and lysosomal+mitochondrial (L+M) fractions
from rats during the early phase of the experimental model of cerulein
(Cer)-induced AP. Subcellular pancreatic extracts from diseased and control
rats were analyzed by 2-DE (3-5.6 pH range) and MALDI-TOF/TOF MS. Comparative
analysis afforded the conclusive identification of 13 (soluble fraction) and 7
(L+M fraction) proteins or protein fragments ocurring in different amounts
between diseased and control pancreas, some of them being newly described in
AP. In the soluble fraction, the authors detected changes related to
inflammation and apoptosis (α1-inhibitor-3, α-1 antitrypsin, α-1
macroglobulin, haptoglobin, STRAP), oxidative stress and stress response
(peroxiredoxin-2, thioredoxin-like 1, GRP94/TRA1, heat shock cognate 71kDa
protein), digestive proteases (elastase 3B), serine protease inhibition
(serpins B6 and A3L) and translation processes (EF 1-δ). In the L+M
fraction, the authors detected changes mainly related to energy generation or
cellular metabolism (ATP synthase β subunit, chymotrypsinogen B,
triacylglycerol lipase), cell redox homeostasis (iodothyronine
5´monodeiodinase) and digestive proteases (carboxypeptidase B1). The data
should provide valuable information for unraveling the early pathophysiologic
mechanisms of Cer-induced AP.
J Pediatr Surg
2012; 47(6):1185-91.
(PMID: 22703791)
Utility of the computed tomography
severity index (Balthazar score) in children with acute pancreatitis
Lautz TB, Turkel G, Radhakrishnan J, Wyers M, Chin AC
Department of Surgery, Children’s Memorial Hospital,
Northwestern University. Chicago, IL, USA
BACKGROUND: Previous studies in children with acute pancreatitis have
demonstrated that clinical scoring systems such as the Ranson, modified
Glasgow, and pediatric acute pancreatitis scores are of value in predicting
severity of the disease. The aim of this study was to determine the predictive
value of the computed tomography severity index (CTSI or Balthazar score) in
pediatric patients. METHODS: All children (≤18 years) admitted to their
institution with acute pancreatitis from 2000 through 2009 were reviewed.
Contrast-enhanced computed tomographic (CT) images at presentation were
retrospectively reviewed by two pediatric radiologists. Peripancreatic fluid
and the extent of necrosis were assessed to determine the CTSI. The predictive
value of the CTSI was calculated and compared with clinical scoring systems.
RESULTS: Of 211 children with acute pancreatitis, 64 underwent
contrast-enhanced CT at presentation. The median age was 12.3 years. Etiology
of pancreatitis was idiopathic (35.9%), gallstone (17.2%), medication-induced
(20.3%), posttransplant (9.4%), traumatic (6.3%), structural (1.6%), and other
(9.4%). The sensitivity, specificity, positive predictive value, and negative
predictive value of the CTSI (using a cutoff score of 4+) were 81%, 76%, 62%,
and 90%, respectively, which compared favorably to the results of the pediatric
acute pancreatitis (53%, 72%, 41%, 80%), Ranson (71%, 87%, 67%, 89%), and modified
Glasgow (71%, 87%, 67%, 89%) scores. CONCLUSION: The CTSI is superior to
clinical scoring systems for identifying children with acute pancreatitis at
heightened risk for developing serious complications.
Dig Dis 2012; 30(3):277-83.
(PMID: 22722552)
The role of chronic inflammation:
chronic pancreatitis as a risk factor of pancreatic cancer
Dítě P, Hermanová M, Trna J, Novotný I,
Růžička M, Liberda M, Bártková A
Faculty of Medicine, University of Ostrava. Ostrava,
Czech Republic
Pancreatic carcinoma is a condition with late diagnosis and one for which
there is no effective screening method. One possible diagnostic approach of
so-called early adenocarcinoma is the identification and systematic examination
of individuals at risk for this condition. Between 1992 and 2005 the authors
systematically observed 223 individuals diagnosed with chronic pancreatitis. In
this 14-year period the authors performed classical biochemical tests,
endoscopic ultrasound, CT scans and ERCP. The authors also asked about the
number of cigarettes smoked per year and classified individuals consuming
regularly more than 80 g of alcohol per day for 5 years for men and 50 g of
alcohol per day for 5 years for women as having the alcoholic form of chronic
pancreatitis. The remaining patients were classified according to the TIGARO
classification. Alcohol-related etiology was detected in 73.1% of patients,
21.5% had the chronic obstructive form and only 5.4% were classified as
idiopathic pancreatitis. Pancreatic carcinoma was detected in 13 patients with
chronic pancreatitis (5.8%), 3 patients were diagnosed with gastric carcinoma
and 1 with esophageal carcinoma. Pancreatic malignancy developed mainly in
patients with the alcoholic form of pancreatitis (4.5%). In the 14-year period
11 subjects died, out of which 8 cases were related to pancreatic carcinoma.
Pancreatic and extrapancreatic cancer localized in the gastrointestinal tract are
serious complications of chronic nonhereditary pancreatitis. Systematic
observation of patients with chronic pancreatitis must be performed with the
aim of early diagnosis of pancreatic malignancies (but also including other
types).
J Gastrointest Surg 2012; Jun 19.
(PMID: 22711213)
The daily practice of pancreatic
enzyme replacement therapy after pancreatic surgery: a Northern European
survey: enzyme replacement after surgery
Sikkens EC, Cahen DL, van Eijck C, Kuipers EJ, Bruno MJ
Department of Gastroenterology and Hepatology, Erasmus
University Medical Center. Rotterdam, The Netherlands
INTRODUCTION: After pancreatic surgery, up to 80% of patients will develop
exocrine insufficiency. For enzyme supplementation to be effective, prescribing
an adequate dose of pancreatic enzymes is mandatory but challenging because the
required dose varies. Data on the practice of enzyme replacement therapy after
surgery are lacking, and therefore, the authors conducted this analysis.
METHODS: An anonymous survey was distributed to members of the Dutch and German
patient associations for pancreatic disorders. The target population consisted
of patients with chronic pancreatitis or pancreatic cancer who had undergone
pancreatic surgery and were using enzymes to treat exocrine insufficiency.
Results were compared to a similar group of non-operated patients. RESULTS:
Ninety-one cases were analyzed (84% underwent a resection procedure). The
median daily enzyme dose was 6, and 25% took three or less capsules. Despite
treatment, 68% of patients reported steatorrhea-related symptoms, 48% adhered
to a non-indicated dietary fat restriction, and only 33% had visited a
dietician. The outcome was equally poor for the 91 non-operated patients.
CONCLUSION: Most patients suffering from exocrine insufficiency after
pancreatic surgery are undertreated. To improve efficacy, physicians should be
more focused on treating exocrine insufficiency and educate patients to adjust
the dose according to symptoms and their diet.
Pancreas 2012;
Jun 12.
(PMID: 22695134)
Changes in 1,25-dihydroxyvitamin D
and 25-hydroxyvitamin D are associated with maturation of regulatory T
lymphocytes in patients with chronic pancreatitis: a randomized controlled
trial
Bang UC, Brandt L, Benfield T, Jensen JE
Department of Endocrinology, Hvidovre Hospital.
Copenhagen, Denmark
OBJECTIVES: The authors studied the impact of changes in 25-hydroxyvitamin
D (25OHD) and 1,25-dihydroxyvitamin D (1,25(OH)2D) on regulatory T lymphocytes
(Tregs) in patients with chronic pancreatitis (CP) and fat malabsorption in a
prospective clinical trial. METHODS: The patients were randomized to 1 of 3
treatments during 10 weeks: weekly UV-B in a tanning bed (group A), 1,520-IU/d
vitamin D supplement (group B), or placebo (group C). A placebo tanning bed was
used in groups B and C. The authors determined the levels of CD4 Tregs
(CD3CD4CD25CD127lowFoxP3) and CD8 Tregs (CD3CD8CD25CD127lowFoxP3), together
with 25OHD and 1,25(OH)2D. For baseline comparisons, the authors included 8
healthy individuals. Of the 30 included patients, 27 (group A, 7 patients;
group B, 9 patients; and group C, 11 patients) completed the protocol. RESULTS:
The baseline levels of CD4 Tregs relative to total CD4 count were higher in 22
patients with CP compared with healthy controls (2.8% vs. 1.9%, P < 0.05) and were comparable for CD8+ Tregs (0.13% vs. 0.05%, P=0.3). Increases in levels
of CD4 Tregs correlated to changes in 1,25(OH)2D (2% per 100 pmol/L, P=0.002)
and 25OHD (3% per 100 nmol/L, P=0.01). CONCLUSIONS: Patients with CP have
elevated relative levels of CD4 Tregs. Increases in 25OHD and 1,25(OH)2D were
both related with increases in levels of Tregs.
Cancer Causes Control 2012; May 22.
(PMID: 22729932)
Selected cancers with increasing
mortality rates by educational attainment in 26 states in the United States,
1993-2007
Jemal A, Simard EP, Xu J, Ma J, Anderson RN
Surveillance Research Program, American Cancer Society.
Atlanta, GA, USA
BACKGROUND: Mortality rates continue to increase for liver, esophagus, and
pancreatic cancers in non-Hispanic whites and for liver cancer in non-Hispanic
blacks. However, the extent to which trends vary by socioeconomic status (SES)
is unknown. METHODS: The authors calculated age-standardized death rates for
liver, esophagus, and pancreas cancers for non-Hispanic whites and non-Hispanic
blacks aged 25-64 years by sex and level of education (≤12, 13-15, and
≥16 years, as a SES proxy) during 1993-2007 using mortality data from 26
states with consistent education information on death certificates. Temporal
trends were evaluated using log-linear regression, and rate ratios (RRs) with
95% confidence intervals (CIs) compared death rates in persons with ≤12
versus ≥16 years of education. RESULTS: Generally, death rates increased
for cancers of the liver, esophagus, and pancreas in non-Hispanic whites and
non-Hispanic blacks (liver cancer only) with ≤12 and 13-15 years of
education, with steeper increases in the least educated group. In contrast,
rates remained stable in persons with ≥16 years of education. During
1993-2007, the RR (rates in ≤12 versus ≥16 years of education)
increased for all three cancers, particularly for liver cancer among men which
increased from 1.76 (95% CI, 1.38-2.25) to 3.23 (95% CI, 2.78-3.75) in
non-Hispanic whites and from 1.28 (95% CI, 0.71-2.30) to 3.64 (95% CI,
2.44-5.44) in non-Hispanic blacks. CONCLUSIONS: The recent increase in
mortality rates for liver, esophagus, and pancreatic cancers in non-Hispanic
whites and for liver cancer in non-Hispanic blacks reflects increases among
those with lower education levels.
Int J Cancer 2012; Jun 22.
(PMID: 22729780)
Oxidative inhibition of Hsp90
disrupts the super-chaperone complex and attenuates pancreatic adenocarcinoma in vitro and in vivo
Sarkar S, Dutta D, Samanta SK, Bhattacharya K, Pal BC, Li
J, et al.
Cancer Biology and Inflammatory Disorder Division;
Council of Scientific and Industrial Research-Indian Institute of Chemical
Biolog. Kolkata, India
Pancreatic cancer is almost always fatal, in part because of its delayed
diagnosis, poor prognosis, rapid progression and chemoresistance. Oncogenic
proteins are stabilized by the Hsp90, making it a potential therapeutic target.
The authors investigated the oxidative stress-mediated dysfunction of Hsp90 and
the hindrance of its chaperonic activity by a carbazole alkaloid, mahanine, as
a strategic therapeutic in pancreatic cancer. Mahanine exhibited
anti-proliferative activity against several pancreatic cancer cell lines
through apoptosis. It induced early accumulation of reactive oxygen species
(ROS) leading to thiol oxidation, aggregation and dysfunction of Hsp90 in
MIAPaCa-2. N-acetyl-L-cysteine prevented mahanine-induced ROS accumulation,
aggregation of Hsp90, degradation of client proteins and cell death. Mahanine
disrupted Hsp90-Cdc37 complex in MIAPaCa-2 as a consequence of ROS generation.
Client proteins were restored by MG132, suggesting a possible role of
ubiquitinylated protein degradation pathway. Surface plasmon resonance study
demonstrated that the rate of interaction of mahanine with recombinant Hsp90 is
in the range of seconds. Molecular dynamics simulation showed its weak
interactions with Hsp90. However, no disruption of the Hsp90-Cdc37 complex was
observed at an early time point, thus ruling out that mahanine directly disrupts
the complex. It did not impede the ATP binding pocket of Hsp90. Mahanine also
reduced in vitro migration and tube
formation in cancer cells. Further, it inhibited orthotopic pancreatic tumour
growth in nude mice. Taken together, these results provide evidence for
mahanine-induced ROS-mediated destabilization of Hsp90 chaperone activity
resulting in Hsp90-Cdc37 disruption leading to apoptosis, suggesting its
potential as a specific target in pancreatic cancer.
Biochim Biophys Acta 2012; Jun 20.
(PMID: 22728049)
Targeting pancreatic cancer stem
cells for cancer therapy
Xia J, Chen C, Chen Z, Miele L, Sarkar FH, Wang Z
Department of Biochemistry and Biology, Bengbu Medical
College. Anhui, PR of China
Pancreatic cancer (PC) is the fourth most frequent cause of cancer death
in the United States. Emerging evidence suggests that pancreatic cancer stem
cells (CSCs) play a crucial role in the development and progression of PC.
Recently, there is increasing evidence showing that chemopreventive agents
commonly known as nutraceuticals could target and eliminate CSCs that has been
proposed as the root of the tumor progression, which could be partly due to
attenuating cell signaling pathways involved in CSCs. Therefore, targeting
pancreatic CSCs by nutraceuticals for the prevention of tumor progression and
treatment of PC may lead to the development of novel strategy for achieving
better treatment outcome of PC patients. In this review article, the authors
have summarized the most recent advances in the pancreatic CSCs field, with
particular emphasis on nutraceuticals to target CSCs for fighting this deadly
disease.
J Clin
Endocrinol Metab 2012; Jun 22.
(PMID: 22730516)
Health disparities in endocrine disorders: biological,
clinical, and nonclinical factors: an Endocrine Society Scientific Statement
Golden SH, Brown A, Cauley JA, Chin MH, Gary-Webb TL, Kim
C, et al.
Department of Medicine, Johns Hopkins University School of
Medicine. Baltimore, MD, USA
The aim was
to provide a scholarly review of the published literature on biological,
clinical, and nonclinical contributors to race/ethnic and sex disparities in
endocrine disorders and to identify current gaps in knowledge as a focus for
future research needs. Participants in Development of Scientific Statement: The
Endocrine Society’s Scientific Statement Task Force (SSTF) selected the leader
of the statement development group. She selected an eight-member writing group
with expertise in endocrinology and health disparities, which was approved by
the Society. All discussions regarding the scientific statement content
occurred via teleconference or written correspondence. No funding was provided
to any expert or peer reviewer, and all participants volunteered their time to
prepare this Scientific Statement. Evidence: The primary sources of data on
global disease prevalence are from the World Health Organization. A
comprehensive literature search of PubMed identified U.S. population-based
studies. Search strategies combining Medical Subject Headings terms and keyword
terms and phrases defined two concepts: 1) racial, ethnic, and sex differences
including specific populations; and 2) the specific endocrine disorder or
condition. The search identified systematic reviews, meta-analyses, large
cohort and population-based studies, and original studies focusing on the
prevalence and determinants of disparities in endocrine disorders. Consensus
Process: The writing group focused on population differences in the highly
prevalent endocrine diseases of type 2 diabetes mellitus and related conditions
(prediabetes and diabetic complications), gestational diabetes, metabolic
syndrome with a focus on obesity and dyslipidemia, thyroid disorders,
osteoporosis, and vitamin D deficiency. Authors reviewed and synthesized
evidence in their areas of expertise. The final statement incorporated
responses to several levels of review: 1) comments of the SSTF and the Advocacy
and Public Outreach Core Committee; and 2) suggestions offered by the Council
and members of The Endocrine Society. Conclusions: Several themes emerged in
the statement, including a need for basic science, population-based,
translational and health services studies to explore underlying mechanisms
contributing to endocrine health disparities. Compared to non-Hispanic whites,
non-Hispanic blacks have worse outcomes and higher mortality from certain
disorders despite having a lower (e.g., macrovascular complications of diabetes
mellitus and osteoporotic fractures) or similar (e.g., thyroid cancer)
incidence of these disorders. Obesity is an important contributor to diabetes
risk in minority populations and to sex disparities in thyroid cancer,
suggesting that population interventions targeting weight loss may favorably
impact a number of endocrine disorders. There are important implications
regarding the definition of obesity in different race/ethnic groups, including
potential underestimation of disease risk in Asian-Americans and overestimation
in non-Hispanic black women. Ethnic-specific cut-points for central obesity
should be determined so that clinicians can adequately assess metabolic risk.
There is little evidence that genetic differences contribute significantly to
race/ethnic disparities in the endocrine disorders examined. Multilevel
interventions have reduced disparities in diabetes care, and these successes
can be modeled to design similar interventions for other endocrine diseases.
IUBMB Life
2012; Jun 23.
(PMID: 22730258)
Metformin reverses hexokinase and phosphofructokinase
downregulation and intracellular distribution in the heart of diabetic mice
Da Silva D, Ausina P, Alencar EM, Coelho WS, Zancan P,
Sola-Penna M
Laboratório de Enzimologia e Controle do
Metabolismo-LabECoM, Faculdade de Farmácia. UFRJ, Brazil
Diabetes
mellitus is characterized by hyperglycemia and its associated complications,
including cardiomyopathy. Metformin, in addition to lowering blood glucose
levels, provides cardioprotection for diabetic subjects. Glycolysis is
essential to cardiac metabolism and its reduction may contribute to diabetic
cardiomyopathy. Hexokinase (HK) and phosphofructokinase (PFK), rate-limiting
enzymes of glycolysis, are downregulated in cardiac muscle from diabetic
subjects, playing a central role on the decreased glucose utilization in the
heart of diabetic subjects. Thus, the aim of this study was to determine
whether metformin modulates heart HK and PFK from diabetic mice. Diabetes was
induced by streptozotocin injection on male Swiss mice, which were treated for
three consecutive days with 250 mg/kg metformin before evaluating HK and PFK
activity, expression, and intracellular distribution on the heart of these
subjects. The authors show that metformin abrogates the downregulation of HK
and PFK in the heart of streptozotocin-induced diabetic mice. This effect is
not correlated to alteration on the enzymes’ transcription and expression.
However, the intracellular distribution of both enzymes is altered in diabetic
hearts that show increased activity of the soluble fraction when compared to
the particulate fraction. Moreover, this pattern is reversed upon the treatment
with metformin, which is correlated with the effects of the drug on the enzymes
activity. Altogether, these results support evidences that metformin alter the
intracellular localization of HK and PFK augmenting glucose utilization by diabetic
hearts and, thus, conferring cardiac protection to diabetic subjects.
Int J
Colorectal Dis 2012; Jun 23.
(PMID: 22729713)
Increased risk of diabetes following perianal abscess: a
population-based follow-up study
Wei PL, Keller JJ, Kuo LJ, Lin HC
Division of General Surgery, Department of Surgery, Taipei
Medical University Hospital. Taipei, Taiwan
PURPOSE: It
remains unclear whether perianal abscess is a prediabetes condition or the
initial presentation of type 2 diabetes. Using a population-based dataset, this
study aimed to explore the risk of type 2
diabetes following perianal abscess. METHODS: The authors used data
sourced from the Longitudinal Health Insurance Database 2000. In total, there
were 1,419 adult patients with perianal abscess in the study group and 7,095
randomly selected subjects in the comparison group. Stratified Cox proportional
hazards regressions were carried out to evaluate the association between being
diagnosed with perianal abscess and receiving a subsequent diagnosis of
diabetes within 5 years. RESULTS: Of the total 8,514 sampled subjects, the
incidence rate of diabetes per 100 person-years was 1.87 (95% confidence
interval (CI)=1.74-2.01); the rate among patients with perianal abscess was
3.00 (95% CI=2.60-3.43) and was 1.65 (95% CI=1.52-1.79) among comparison
patients. Stratified Cox proportional hazards analysis revealed that patients
with perianal abscess were more likely to have received a diagnosis of diabetes
than comparison patients (hazard ratio=1.80, 95% CI=1.50-2.16, P<0.001)
during the 5-year follow-up period after censoring cases that died from
nondiabetes causes and adjusting for patient geographic location, urbanization
level, monthly income, hypertension, coronary heart disease, hyperlipidemia,
obesity, and alcohol abuse/alcohol dependence syndrome at baseline.
CONCLUSIONS: These results suggest that patients with perianal abscess have a
higher chance of contracting type 2 diabetes mellitus within the first 5 years
following their diagnosis.
Protein Cell
2012; Jun 22.
(PMID: 22729395)
Mitochondria in the pathogenesis of diabetes: a proteomic
view
Chen X, Wei S, Yang F.
Key Laboratory of Protein and Peptide Pharmaceuticals and
Laboratory of Proteomics, Institute of Biophysics, Chinese Academy of Sciences.
Beijing, PR of China
Diabetes
mellitus is a complex metabolic disorder characterized by chronic hyperglycemia
due to absolute or relative lack of insulin. Though great efforts have been
made to investigate the pathogenesis of diabetes, the underlying mechanism
behind the development of diabetes and its complications remains unexplored.
Cumulative evidence has linked mitochondrial modification to the pathogenesis
of diabetes and its complications and they are also observed in various tissues
affected by diabetes. Proteomics is an attractive tool for the study of
diabetes since it allows researchers to compare normal and diabetic samples by
identifying and quantifying the differentially expressed proteins in tissues,
cells or organelles. Great progress has already been made in mitochondrial
proteomics to elucidate the role of mitochondria in the pathogenesis of
diabetes and its complications. Further studies on the changes of mitochondrial
protein specifically post-translational modifications during the diabetic state
using proteomic tools, would provide more information to better understand
diabetes.