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

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*

BACKGROUND: Recent studies of thromboelastograph (TEG) findings have revealed that the hemostatic process is enhanced in uremic patients, suggesting an increased risk of thrombosis formation. The pathogenesis of hypercoagulability appears to be multifactorial in origin, and to involve associated lipid metabolism abnormalities. The purpose of this study was to investigate changes in TEG findings and lipid metabolism after renal transplantation. METHODS: 23 patients scheduled for renal transplantation were included. PT, PT-INR, and aPTT were used as laboratory blood coagulation tests, and concentrations of triglyceride and total cholesterol as indices of lipid metabolism abnormalities. TEG variables were measured before renal transplantation, and again at one and three weeks after transplantation, and then compared with pre-transplantation values. RESULTS: The pre-transplantation values of alpha-angle, maximal amplitude and A60 were above the normal ranges, showing hypercoagulability. They reduced significantly after successful transplantation suggesting that the hypercoagulable tendency is relieved upon correcting uremia (P < 0.05). The lipid metabolism study showed hypertriglyceridemia before transplantation. Triglyceride concentrations reduced significantly to normal levels after renal transplantation (P < 0.05), and were correlated with changes in alpha-angle, maximal amplitude, A60, TEG index, and LY30 (P < 0.01). CONCLUSIONS: Patients with chronic renal failure, associated with hypertriglyceridemia, as a form of lipid metabolism abnormality, showed hypercoagulability on TEG. With the correction of uremia after renal transplantation, the hypercoagulable findings are relieved and triglyceride levels reduce to normal. The normalization of lipid metabolism after renal transplantation might have a participatory role in relieving hypercoagulability.
Blood Coagulation Tests ; Cholesterol ; Humans ; Hyperlipidemias ; Hypertriglyceridemia ; Kidney Failure, Chronic* ; Kidney Transplantation* ; Lipid Metabolism ; Reference Values ; Thrombophilia ; Thrombosis ; Triglycerides ; Uremia

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

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

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: The increased prevalence of dyslipoproteinemia in obese children probably contributes to the high risk of cardiovascular disease associated with being overweight. The genetic makeup is possible one of the factors that influence the impact of obesity on lipid metabolism. A relation between apolipoprotein E (Apo E) polymorphism and lipid metabolism has been convincingly demonstrated in large population. The purpose of this study was to determine whether Apo E polymorphism also influences the risk of dyslipidemia in obese children. METHODS: We studied 89 obese children with weight-for-height excess of 40% by obesity index. We measured the serum concentration of total cholesterol, triglyceride, HDL-cholesterol, LDL- cholesterol, Lipoprotein (a) (Lp(a)), apolipoprotein A (Apo A) and Apo B after overnight fasting. Apo E gene polymorphism of the 89 obese children and 30 control students were analyzed by ARMS (amplication refractory mutation system) method. RESULTS: The frequency of etsilon2, etsilon3, and etsilon4 allele were 9.7%, 82.3% and 8.0%, respectively in children. There was no significant difference between Apo E allele frequency of obese children and those of nonobese children. The serum concentrations of total cholesterol, LDL-cholesterol and Apo B were lower in etsilon2 genotype. The obese children with etsilon4 genotype had higher frequency of hypertriglyceridemia, increased level of Lp(a) and decreased level of HDL-cholesterol than other types. There was no evidence of EKG abnormality and cardiovascular complications in obese children. CONCLUSION: Our data demonstrated that obesity is associated with an increase in the risk of lipoprotein abnormalities and that the serum concentrations of total cholesterol, LDL-cholesterol and Apo B were influenced by Apo E genotypes.
Alleles ; Apolipoproteins B ; Apolipoproteins E ; Apolipoproteins* ; Arm ; Cardiovascular Diseases ; Child* ; Cholesterol ; Dyslipidemias ; Electrocardiography ; Fasting ; Gene Frequency ; Genotype ; Humans ; Hypertriglyceridemia ; Lipid Metabolism ; Lipoprotein(a) ; Lipoproteins ; Obesity ; Overweight ; Plasma* ; Prevalence ; Triglycerides

PURPOSE: Weight changes, especially weight gain, is a side effect of antiepileptics(especially valproate and carbamazepine). This may be sufficiently severe to cause noncompliance or to require the withdrawal of effective treatment. Unfortunately, the exact mechanism of weight change is not illustrated. Several reports and our experiment suggested that weight gain highly correlated with a familial tendency of obesity. The genetic makeup is a possible factor among those of the factors that influence the impact of obesity on lipid metabolism. The purpose of this prospective, random trial clinical study was to evaluate the coherence between the changes of weight and lipid profiles and apolipoprotein E polymorphism in children with antiepileptics. METHODS: We studied 60 epileptic children treated with antiepileptics. We measured the body mass index and lipid profiles:total cholesterol, triglyceride, HDL-cholesterol and LDL-cholesterol. Changes of appetite and family histories of obesity were examined. The apolipoprotein E gene polymorphisms of the patients were analyzed by the amplification refractory mutation system method. RESULTS: The body mass indexes of patient were significantly increased in all patient groups. The epileptic children who had E4 genotype showed higher frequencies of hypertriglyceridemia, hypercholesterolemia, and decreased level of HDL-cholesterol than other types. There was no significant difference between Apo E subtype with family histories of obesity and body mass index. CONCLUSION: An association with Apo E4 genotype and changes of serum lipid were demonstrated significantly in children on antiepileptics. But there was no significant difference between Apo E subtype and body mass index.
Anticonvulsants* ; Apolipoprotein E4 ; Apolipoproteins E ; Apolipoproteins* ; Appetite ; Body Mass Index ; Body Weight* ; Child* ; Cholesterol ; Genotype ; Humans ; Hypercholesterolemia ; Hypertriglyceridemia ; Lipid Metabolism ; Obesity ; Prospective Studies ; Triglycerides ; Valproic Acid ; Weight Gain

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

Familial combined hyperlipidemia is one af the manogenic disorders frequently found in humans and is seen in 0.5~2% of the general populatian, accounting for at least 10% of persons with pemature atlmmcletusis. The distinguishing feature of familial combined hyperlipidemia, in camparison with other single-gene abnarmalities of lipoprotein metabolism, is that not all affected members have the same plasma lipid phenotype; some individuals have an elevation of cholesterol concentration alane(type IIa lipoprotein pattern), while some athers have an elevation of triglyceride concentration alone(type IV pattem), and still others have elevations of both values(type IIb pattem). In any one persan, the lipid phenotype can change as a result of dietary or drug treatment. Familial combined hyperlipidemia should be suspected in those subjects with moderate hypertriglyceridemia and/or moderate hypercholestaolemia (lipoprotein types IIa, Ilb, IV), especially when premature coronary heart disease is evident in the family histary. Low plasma HDL-cholesterol, obesity, insulin resistance and hyperuricemia are often . Family members affected by familial combined hyperlipidemia should be identified and be treated, since tbe condition is associated with premature caronary heart diasease. We have found one family of familial combined hyperlipidemia with one member(case 1) associated with insulin resistance, hyperuricemia and gout, and another member(case 2) associated with diabetes mellitus and infertiTity.
Cholesterol ; Coronary Disease ; Diabetes Mellitus ; Gout ; Heart ; Humans ; Hyperlipidemia, Familial Combined* ; Hypertriglyceridemia ; Hyperuricemia ; Insulin Resistance ; Lipoproteins ; Metabolism ; Obesity ; Phenotype ; Plasma ; Triglycerides