As a member of the apolipoprotein C (ApoC) family with a relatively high content, ApoC3 plays a major role in the regulation of triglyceride metabolism, and plays an important role in the occurrence and development of cardiovascular diseases, glucose and lipid metabolism disorders. Nonalcoholic fatty liver disease (NAFLD) refers to the accumulation of a large amount of fat in the liver in the absence of a history of chronic alcohol consumption or other damage to the liver. A large number of previous studies have shown that there is a correlation between the gene polymorphism and high expression of ApoC3 and NAFLD. In the context of hypertriglyceridemia (HTG), this article reviews the relationship between ApoC3 and NAFLD, glucose and lipid metabolism, and islet β cell function, showing that ApoC3 can not only inhibit lipoprotein lipase (LPL) and hepatic lipase (HL) activity, delay the decomposition of triglyceride in plasma to maintain the body's energy metabolism during fasting, but also be significantly increased under insulin resistance, prompting the liver to secrete a large amount of very low-density lipoprotein (VLDL) to induce HTG. Therefore, targeting and inhibiting ApoC3 might become a new approach to treat HTG. Increasing evidence suggests that ApoC3 does not appear to be an independent "contributor" to NAFLD. Similarly, our previous studies have shown that ApoC3 is not an independent factor triggering islet β cell dysfunction in ApoC3 transgenic mice, but in a state of excess nutrition, HTG triggered by ApoC3 high expression may exacerbate the effects of hyperglycemia and insulin resistance on islet β cell function, and the underlying mechanism remains to be further discussed.
Apolipoprotein C-III/genetics* ; Non-alcoholic Fatty Liver Disease/pathology* ; Glucose/metabolism* ; Lipid Metabolism ; Humans ; Animals ; Hypertriglyceridemia/metabolism* ; Islets of Langerhans/metabolism*

Glucose and lipid metabolism are linked to each other in many ways. The most important clinical manifestation of this interaction is diabetic dyslipidemia, characterized by elevated triglycerides, low high density lipoprotein cholesterol (HDL-C), and predominance of small-dense LDL particles. However, in the last decade we have learned that the interaction is much more complex. Hypertriglyceridemia and low HDL-C cannot only be the consequence but also the cause of a disturbed glucose metabolism. Furthermore, it is now well established that statins are associated with a small but significant increase in the risk for new onset diabetes. The underlying mechanisms are not completely understood but modulation of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG CoA)-reductase may play a central role as genetic data indicate that mutations resulting in lower HMG CoA-reductase activity are also associated with obesity, higher glucose concentrations and diabetes. Very interestingly, this statin induced increased risk for new onset type 2 diabetes is not detectable in subjects with familial hypercholesterolemia. Furthermore, patients with familial hypercholesterolemia seem to have a lower risk for type 2 diabetes, a phenomenon which seems to be dose-dependent (the higher the low density lipoprotein cholesterol, the lower the risk). Whether there is also an interaction between lipoprotein(a) and diabetes is still a matter of debate.
Cholesterol, HDL ; Cholesterol, LDL ; Diabetes Mellitus ; Dyslipidemias* ; Glucose* ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Hyperlipoproteinemia Type II ; Hyperlipoproteinemias ; Hypertriglyceridemia ; Lipid Metabolism* ; Lipoprotein(a) ; Metabolism ; Obesity ; Triglycerides

Sunitinib is a multi-target tyrosine kinase inhibitor used to treat gastrointestinal stromal tumors, renal cell carcinoma, and pancreatic neuroendocrine tumors. The most common adverse reactions are known to be nausea, fatigue, diarrhea, stomatitis, esophagitis, hypertension, skin toxicity (hand-foot syndrome), hypothyroidism, and reduction in the cardiac output of the left ventricle. Herein, we report the case of a 57 year-old female who visited our hospital complaining of epigastric pain. She had been taking sunitinib at 25 mg/day to treat a metastatic pancreatic neuroendocrine tumor. Upon computed tomography performed on admission, we observed that fluid had collected around the pancreas. Laboratory analysis revealed hypertriglyceridemia (triglycerides 993 mg/dL). Tyrosine kinase inhibitors are known to have limited effects on lipid metabolism. In this case, we suggest that hyperglycemia seems to have had a limited effect on lipid levels. We are rather of the view that hyperglycemia, a history of distal pancreatectomy, and hypothyrodisim, indirectly caused the observed hypertriglyceridemia.
Carcinoma, Renal Cell ; Cardiac Output ; Diarrhea ; Esophagitis ; Fatigue ; Female ; Gastrointestinal Stromal Tumors ; Heart Ventricles ; Humans ; Hyperglycemia ; Hypertension ; Hypertriglyceridemia* ; Hypothyroidism ; Lipid Metabolism ; Nausea ; Neuroendocrine Tumors* ; Pancreas ; Pancreatectomy ; Protein-Tyrosine Kinases ; Skin ; Stomatitis

PURPOSE: Preterm infants on parenteral nutrition are at a relatively high risk for hypertriglyceridemia because they have immature lipoprotein lipase activity. The purpose of this study was to analyze the clinical factors affecting lipid metabolism in preterm infants receiving parenteral nutrition and to evaluate the influence of intravenous heparin on serum triglycerides to determine the adequate heparin dose to prevent hypertriglyceridemia in preterm infants. METHODS: A single-center retrospective review was conducted among preterm infants receiving parenteral nutrition between January 2006 and February 2011. In 75 patients, 110 determinations were performed within 28 days postnatal age. Demographic and clinical data, including laboratory parameters, the dose and the duration of lipid administration, and the amount of intravenous heparin, were analyzed. RESULTS: Serum triglycerides were higher in the small for gestational age (SGA) infants than in the appropriate for gestational age infants (185.5+/-134.9 mg/dL vs. 126.9+/-101.9 mg/dL, p=0.019). Birth weight, gestational age, and body weight were negatively correlated with serum triglyceride level (r=-0.289, p=0.002; r=-0.208, p=0.029; r=-0.287, p=0.002, respectively). The serum triglyceride level was statistically lower in preterm infants receiving 1 U/mL of heparin than in those receiving 0.5 U/mL heparin or no heparin. CONCLUSION: Preterm infants receiving parenteral nutrition, particularly SGA and extremely low birth weight infants, tend to have hypertriglyceridemia. Thus, administration of 1 U/mL of heparin rather than 0.5 U/mL or none may be helpful to prevent hypertriglyceridemia in preterm infants.
Birth Weight ; Body Weight ; Gestational Age ; Heparin ; Humans ; Hypertriglyceridemia ; Infant ; Infant, Low Birth Weight ; Infant, Newborn ; Infant, Premature ; Lipid Metabolism ; Lipoprotein Lipase ; Parenteral Nutrition ; Retrospective Studies ; Triglycerides

Obesity is defined as BMI (calculated as weight in kg divided by height in m2) more than 30, and overweight is defined as BMI of 25-29.9. Obesity has been considered as a risk factor for pancreatic diseases, including pancreatitis and pancreatic cancer. Severe acute pancreatitis is significantly more frequent in obese patients. Furthermore, obese patients develop systemic and local complications of acute pancreatitis more frequently. The underlying mechanisms are increased inflammation and necrosis from increased amount of intra- and peri-pancreatic fat. In addition, obesity is a poor prognostic factor in acute pancreatitis, and overweight before disease onset appears to be a risk factor for chronic pancreatitis. Overweight and/or obesity are associated with greater risk of pancreatic cancer and younger age of onset. Physical activity appears to decrease the risk of pancreatic cancer, especially among those who are overweight. Long-standing diabetes increases the risk of pancreatic cancer. The pathogenic mechanism is that obesity and physical inactivity increase insulin resistance. In a state of hypersinulinemia, increased circulating level of insulin-like growth factor-1 induces cellular proliferation of pancreatic cancer. Obesity is associated with negative prognostic factor and increased mortality in pancreatic cancer. However, there are controversies regarding the effects of obesity on long-term post-operative results in the patient with pancreatic cancer.
Body Mass Index ; Humans ; Hypertriglyceridemia/complications ; Obesity/*complications ; Overweight ; Oxidative Stress ; Pancreatic Diseases/*etiology ; Pancreatic Neoplasms/etiology ; Somatomedins/metabolism/physiology

OBJECTIVETo determine whether smoking increases the risk for developing metabolic syndrome (MetS) in Chinese men.

METHODSA total of 693 men with no MetS at baseline were followed for 2.9-5.5 years. Subjects were divided into nonsmokers, ex-smokers, and current smokers according to baseline smoking status.

RESULTSAfter adjusting for age, education level, alcohol intake, fasting plasma insulin, HOMA-IR index, and BMI at baseline and weight change, current smokers were dose-dependently associated with increased risk for developing new MetS compared with nonsmokers. The odds ratio (OR) was 2.131 (95% CI, 1.264, 3.592; P<0.01) for the NCEPIII definition or 3.083 (95% CI, 1.807, 5.295; P<0.01) for the JCDCG definition of MetS. Ex-smokers who had quit for ≥13 years significantly decreased the risk for developing new MetS defined by the JCDCG definition. Compared with nonsmokers, current smokers were significantly associated with increased incidence of hypertriglyceridemia and low HDL-C.

CONCLUSIONSmoking is a risk factor for developing MetS in Chinese men after adjusting for age, education level, alcohol intake, fasting plasma insulin, HOMA-IR, BMI, and weight change. This could be due to an increased incidence of dyslipidemia. Smoking cessation for >13 years decreased the risk for developing MetS defined by the JCDCG definition.

Adult ; Aged ; Aged, 80 and over ; Blood Glucose ; metabolism ; Body Mass Index ; China ; epidemiology ; Cholesterol, HDL ; blood ; Diabetes Mellitus ; blood ; epidemiology ; Follow-Up Studies ; Humans ; Hypertriglyceridemia ; blood ; epidemiology ; Male ; Metabolic Syndrome ; blood ; epidemiology ; etiology ; Middle Aged ; Odds Ratio ; Risk Factors ; Smoking ; adverse effects ; blood ; epidemiology ; Waist Circumference

Hypertriglyceridemia is a rare cause of pancreatitis in pregnancy. Pregnancy is related with hypertriglyceridemia especially in the 3rd trimester due to increase of estrogen. Diabetes is known as a common cause of secondary lipid metabolism disorder and is often associated with hypertriglyceridemia. Shock and sepsis related to pancreatitis in pregnancy result in a relatively high morbidity and mortality rate for both the mother and the fetus. Hypertriglyceridemic pancreatitis complicated in gestational diabetes has not previously been reported. We report a case of 26(+4) weeks gestational aged primigravida with acute pancreatitis induced by hypertriglyceridemia in gestational diabetes. We reviewed the clinical courses and treatments of acute pancreatitis in pregnancy with the literatures.
Aged ; Diabetes, Gestational ; Estrogens ; Female ; Fetus ; Humans ; Hypertriglyceridemia ; Lipid Metabolism Disorders ; Mothers ; Pancreatitis ; Pregnancy ; Sepsis ; Shock

PURPOSE: This study sought to determine whether abdominal obesity is a risk factor for impaired fasting glucose (IFG) and hypertriglyceridemia and to verify whether moderate effect of abdominal obesity on the relationship between IFG and hypertriglyceridemia in Korea. MATERIALS AND METHODS: Data from the Korean National Health and Nutrition Examination Survey was used for the analysis. The study population included 5,938 subjects aged 20 year old drawn from non-diabetic participants in a health examination survey. The subjects were classified according to the presence of abdominal obesity based on waist circumference, IFG based on their fasting blood glucose level, and hypertriglyceridemia on their fasting triglyceride. RESULTS: The multivariate-adjusted odds ratios for the occurrence of hypertriglyceridemia were 2.91 in the abdominal obesity group as compared with the nonobesity group and 1.31 in subjects with IFG compared with the normoglycemia controls. Abdominal obesity was found to be positively moderated in the interaction between waist circumference and fasting blood sugar. CONCLUSION: The moderate effect between abdominal obesity and IFG contributes to the development of hypertriglyceridemia in Korea.
Adult ; Aged ; Blood Glucose/*metabolism ; Fasting/blood ; Female ; Humans ; Hypertriglyceridemia/*blood/*pathology ; Logistic Models ; Male ; Middle Aged ; Obesity, Abdominal/*physiopathology ; Triglycerides/blood ; Waist Circumference/physiology ; Young Adult

OBJECTIVETo investigate effects of medium- and long-chain fatty acid triacylglycerols (MLCT) on body fat and serum lipid in overweight and hypertriglyceridemic subjects.

METHODSA double-blind, controlled clinical trial was carried out, in which 112 subjects with hypertriglyceridemia were enrolled and divided into two groups, there were 56 subjects in each group. One group was randomized to consume long-chain fatty acid triacylglycerol (LCT), and the other to MLCT. All volunteers were asked to consume 25 - 30 g test oil daily for consecutive 8 weeks. Anthropometric measurements of body weight, body fat weight, waist circumference(WC), hip circumference(HC), WHR (ratio of WC/HC), total fat weight, subcutaneous fat area, visceral fat area, and serum biochemical variables of glucose, total cholesterols(TC), triglycerides(TG), high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C)were measured at the initial and final time of the study.

RESULTS11 subjects were excluded from the study because of various reasons. Of the 101 included cases, there were 50 (male subject 34, 68.0%) and 51 (male subject 33, 64.7%) subjects left in LCT and MLCT group respectively. The proportion of men in MLCT (64.7%, 33/51) was not significantly different (chi(2) = 0.1227, P > 0.05) compared to those in LCT (68.0%, 34/50). The average age of MLCT was (54.2 +/- 12.5) which was not significantly different (t = 0.39, P > 0.05) compared to those in LCT (53.2 +/- 13.0); Body mass index (BMI) of MLCT was (25.9 +/- 3.3) kg/m(2), which was not significantly different (t = 0.08, P > 0.05) compared to those of LCT (25.9 +/- 2.4) kg/m(2). After consumption of test oil for 8 weeks, extent of decrease in BMI, percent of body fat, subcutaneous fat, serum TG and serum LDL-C in overweight subjects of MLCT were (-0.73 +/- 0.61) kg/m(2), (-1.53 +/- 1.32)%, (-16.29 +/- 19.25) cm(2), (-0.57 +/- 0.86) mmol/L and (-0.05 +/- 0.64) mmol/L respectively, those in overweight subjects of LCT were (-0.19 +/- 0.61) kg/m(2), (-0.58 +/- 1.02)%, (4.69 +/- 19.06) cm(2), (0.65 +/- 1.10) mmol/L and (0.38 +/- 0.58) mmol/L respectively, all of them were significantly different (the value of t were -2.70, -2.43, -3.20, -3.81 and -2.09 respectively, all of P value were less than 0.05).

CONCLUSIONConsumption of MLCT can reduce body fat weight and serum triacylglycerol and LDL-C in overweight hypertriglyceridemic subjects under an appropriate dietary regime.

Adipose Tissue ; metabolism ; Adult ; Aged ; Double-Blind Method ; Fatty Acids ; therapeutic use ; Female ; Humans ; Hypertriglyceridemia ; diet therapy ; metabolism ; Lipids ; blood ; Male ; Middle Aged ; Overweight ; Triglycerides ; blood

PURPOSE: To report a case of a familial lecithin cholesterol acyltransferase (LCAT) deficiency patient with bilateral corneal opacities. CASE SUMMARY: A 26-year-old man with bilateral corneal opacities visited our hospital. We took slit lamp examination, corneal thickness measurement, corneal endothelial cell counts and fundus examination. Blood and urine tests were included. Kidney biopsy was done. The tissues were observed by a light microscopy and an electron microscopy. Hemolytic anemia, proteinuria, hematuria, hypertriglyceridemia, decreased HDL cholesterol level, and lecithin cholesterol acyltransferase (LCAT) deficiency were found. At kidney biopsy, electron-lucent vacuoles and lamellar inclusion body were found. CONCLUSIONS: Bilateral corneal opacities can be an imporant clinical sign of systemic disease which is caused by abnormal lipid metabolism like the familial lecithin cholesterol acyltransferase (LCAT) deficiency.
Adult ; Anemia, Hemolytic ; Biopsy ; Cholesterol, HDL ; Corneal Opacity ; Corneal Pachymetry ; Endothelial Cells ; Hematuria ; Humans ; Hypertriglyceridemia ; Inclusion Bodies ; Kidney ; Light ; Lipid Metabolism ; Microscopy ; Microscopy, Electron ; Phosphatidylcholine-Sterol O-Acyltransferase ; Proteinuria ; Vacuoles