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Effect of green tea extract on lipid profile in patients with type 2 diabetes mellitus: A systematic review and meta-analysis.
Asbaghi, O, Fouladvand, F, Moradi, S, Ashtary-Larky, D, Choghakhori, R, Abbasnezhad, A
Diabetes & metabolic syndrome. 2020;(4):293-301
Abstract
BACKGROUND Previous studies have indicated controversial results regarding the efficacy of green tea extract (GTE) in improving the lipid profile of type 2 diabetes mellitus (T2DM) patients. We aimed to conduct a systematic review and meta-analysis to pool data from randomized controlled trials (RCTs). METHODS A systematic search was performed in Web of Science, PubMed, and Scopus databases, without any language and time restriction until August 2019, to retrieve the RCTs which examined the effects of GTE on serum concentrations of high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglyceride (TG) or total cholesterol (TC) in T2DM patients. Meta-analyses were carried out using a random effects model. I2 index was used to evaluate the heterogeneity. RESULTS Initial search yielded 780 publications. Of these, seven studies were eligible. The supplementary intake of GTE improved lipid profile by reducing serum TG concentrations in patients with T2DM. Meanwhile, subgroup analyses based on duration of interventions (≤8 and > 8 weeks) and intervention dosage (≤800 and > 800 mg/day) showed that the GTE supplementation longer than 8 weeks and in doses >800 mg/day resulted in a significant decrease in serum TG concentrations. Furthermore, intervention longer than 8 weeks with doses lower than 800 mg/day resulted in a significant reduction in serum TC concentrations. CONCLUSION In conclusion, present systematic review and meta-analysis revealed that the supplementary intake of GTE may improve lipid profile by reducing serum concentrations of TG in patients with T2DM. Furthermore, the results of our stratified analyses suggested that long-term GTE intervention may reduce serum concentrations of TG and TC.
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Pharmacological Effects of Niacin on Acute Hyperlipemia.
la Paz, SM, Bermudez, B, Naranjo, MC, Lopez, S, Abia, R, Muriana, FJ
Current medicinal chemistry. 2016;(25):2826-2835
Abstract
The well-known changes in modern lifestyle habits including over nutrition and physical inactivity have led to striking adverse effects on public health (e.g., obesity, diabetes, and metabolic syndrome) over recent decades. One noticeable consequence is exaggerated and prolonged state of postprandial hyperlipemia due to the ingestion of multiple fat-enriched meals during the course of a day. Postprandial (non-fasting) hyperlipemia is characterized by increased blood levels of exogenous triglycerides (TG) in the form of apolipoprotein (apo) B48-containing TG-rich lipoproteins (TRL), which have a causal role in the pathogenesis and progression of cardiovascular disease (CVD). The cardiovascular benefits of lifestyle modification (healthy diet and exercise) and conventional lipid-lowering therapies (e.g., statins, fibrates, and niacin) could involve their favourable effects on postprandial metabolism. Pharmacologically, niacin has been used as an athero-protective drug for five decades. Studies have since shown that niacin may decrease fasting levels of plasma verylow- density lipoproteins (VLDL), low-density lipoprotein cholesterol (LDL-C), and lipoprotein [a] (Lp[a]), while may increase high-density lipoprotein cholesterol (HDL-C). Herein, the purpose of this review was to provide an update on effects and mechanisms related to the pharmacological actions of niacin on acute hyperlipemia.
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Lipids in hepatic glycogen storage diseases: pathophysiology, monitoring of dietary management and future directions.
Derks, TG, van Rijn, M
Journal of inherited metabolic disease. 2015;(3):537-43
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Abstract
Hepatic glycogen storage diseases (GSD) underscore the intimate relationship between carbohydrate and lipid metabolism. The hyperlipidemias in hepatic GSD reflect perturbed intracellular metabolism, providing biomarkers in blood to monitor dietary management. In different types of GSD, hyperlipidemias are of a different origin. Hypertriglyceridemia is most prominent in GSD type Ia and associated with long-term outcome morbidity, like pancreatitis and hepatic adenomas. In the ketotic subtypes of GSD, hypertriglyceridemia reflects the age-dependent fasting intolerance, secondary lipolysis and increased mitochondrial fatty acid oxidation. The role of high protein diets is established for ketotic types of GSD, but non-traditional dietary interventions (like medium-chain triglycerides and the ketogenic diet) in hepatic GSD are still controversial and necessitate further studies. Patients with these rare inherited disorders of carbohydrate metabolism meet several criteria of the metabolic syndrome, therefore close monitoring for cardiovascular diseases in ageing GSD patients may be justified.
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Epidemiological modifiers of non-alcoholic fatty liver disease: Focus on high-risk groups.
, , Lonardo, A, Bellentani, S, Argo, CK, Ballestri, S, Byrne, CD, Caldwell, SH, Cortez-Pinto, H, Grieco, A, Machado, MV, et al
Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver. 2015;(12):997-1006
Abstract
An improved understanding of non-alcoholic fatty liver disease epidemiology would lead to identification of individuals at high risk of developing chronic liver disease and extra-hepatic complications, thus contributing to more effective case finding of non-alcoholic fatty liver disease among selected groups. We aimed to illustrate the epidemiology of non-alcoholic fatty liver disease in high-risk groups, which were identified based on existing literature. To this end, PubMed was searched to retrieve original articles published until May 2015 using relevant and pertinent keywords "nonalcoholic fatty liver disease" and "diabetes", "obesity", "hyperlipidaemia", "familial heterozygous hypobetalipoproteinaemia", "hypertension", "metabolic syndrome", "ethnicity", "family history" or "genetic polymorphisms". We found that age, sex and ethnicity are major physiological modifiers of the risk of non-alcoholic fatty liver disease, along with belonging to "non-alcoholic fatty liver disease families" and carrying risk alleles for selected genetic polymorphisms. Metabolic syndrome, diabetes, obesity, mixed hyperlipidaemia and hypocholesterolaemia due to familial hypobetalipoproteinaemia are the major metabolic modifiers of non-alcoholic fatty liver disease risk. Compared with these metabolic conditions, however, arterial hypertension appears to carry a relatively more modest risk of non-alcoholic fatty liver disease. A better understanding of the epidemiology of non-alcoholic fatty liver disease may result in a more liberal policy of case finding among high-risk groups.
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Abdominal visceral and subcutaneous fat increase, insulin resistance and hyperlipidemia in testicular cancer patients treated with cisplatin-based chemotherapy.
Willemse, PM, van der Meer, RW, Burggraaf, J, van Elderen, SG, de Kam, ML, de Roos, A, Lamb, HJ, Osanto, S
Acta oncologica (Stockholm, Sweden). 2014;(3):351-60
Abstract
BACKGROUND Testicular cancer survivors treated with chemotherapy are at increased risk for metabolic syndrome (MetS) and cardiovascular disease (CVD). We explored acute effects of chemotherapy by assessing metabolic factors, abdominal fat volume, hepatic triglyceride content (HTC) and aortic wall stiffness. MATERIAL AND METHODS We studied 19 testicular cancer patients (age 20-54 years) before, at three and nine months after the start of chemotherapy. Blood serum was analyzed for lipids, glucose and insulin. Abdominal visceral and subcutaneous fat volume and aortic pulse wave velocity were assessed by magnetic resonance imaging (MRI) techniques; HTC was measured by proton MR spectroscopy. RESULTS Three months after start of chemotherapy visceral abdominal fat volume had significantly increased from 202 ± 141 to 237 ± 153 ml (p = 0.009) whereas body mass index and subcutaneous fat volume significantly increased nine months after treatment from 24.4 ± 4.0 to 26.4 ± 4.1 kg/m(2) (p = 0.01) and from 556 ± 394 to 668 ± 460 ml (p = 0.002) respectively. Serum total cholesterol, low-density lipoprotein cholesterol and insulin also significantly increased three months after start of treatment from 4.88 ± 1.1 to 5.61 ± 1.50 mmol/l (p = 0.002), 3.31 ± 1.16 to 3.73 ± 1.41 mmol/l (p = 0.02) and 5.7 ± 4.4 to 9.6 ± 6.3 mU/ml (p = 0.03), respectively. Nine months after start of chemotherapy serum lipid and insulin concentrations had returned to baseline. HTC increased in seven of the 19 patients (36.8%) during follow-up. Aortic pulse wave velocity remained unchanged at the three time points measured. CONCLUSION Cisplatin-based chemotherapy was associated with acute insulin resistance, dyslipidemia and an immediate increase in abdominal visceral adipose tissue and abdominal subcutaneous adipose tissue in testicular cancer patients. A large prospective cohort study with long follow-up is warranted to characterize the time course and relationship between acutely induced obesity and hypercholesterolemia and the development of metabolic syndrome and CVD years later in individual testicular cancer survivors.
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Effects of hyperlipidaemia on glucocorticoid metabolism: results of a randomized controlled trial in healthy young women.
Mai, K, Reinecke, F, Andres, J, Bobbert, T, Kraatz, J, Wudy, SA, Hartmann, MF, Maser-Gluth, C, Pfeiffer, AF, Spranger, J
Clinical endocrinology. 2011;(5):551-7
Abstract
OBJECTIVE It is well established that the hypothalamic-pituitary-adrenal (HPA) axis is altered in obese individuals. Hyperlipidaemia with elevated levels of free fatty acids (FFAs) is also frequently seen in obesity and in the metabolic syndrome. We hypothesized, therefore, that hyperlipidaemia may alter the activity of the HPA axis. PATIENTS AND METHODS The effects of hyperlipidaemia, including increased circulating FFAs, on ACTH secretion and cortisol metabolism were analysed in 13 healthy young women during the early follicular phase of two subsequent cycles. We administered a 20% lipid/heparin (LHI) or a saline/heparin infusion (SHI) using a crossover design in random order for 330 min. A detailed characterization of glucocorticoid metabolism was performed by measurement of plasma ACTH, cortisol and urinary excretion rates of adrenal glucocorticoids and the glucocorticoid metabolites. RESULTS We observed that LHI-induced hyperlipidaemia elevated serum cortisol levels compared to SHI. No changes in plasma ACTH levels, daily urinary excretion rates of adrenal glucocorticoids, glucocorticoid precursors/metabolites and the calculated activities of the 5α-reductase, 3β-hydroxysteroid dehydrogenase (HSD), 11-, 17-, 21-hydroxylase and 11β-HSD 1 or 2 were found. CONCLUSION Our randomized controlled trial suggests that the adrenal sensitivity to ACTH may be enhanced by LHI-induced hyperlipidaemia in normal-weight healthy young women. This effect might contribute to the disturbances of the HPA axis described in women with abdominal obesity and impaired lipid metabolism.
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Exchanging saturated fatty acids for (n-6) polyunsaturated fatty acids in a mixed meal may decrease postprandial lipemia and markers of inflammation and endothelial activity in overweight men.
Masson, CJ, Mensink, RP
The Journal of nutrition. 2011;(5):816-21
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Postprandial lipemia, low-grade systemic inflammation, and endothelial activity are related to metabolic disorders. It is well known that dietary fatty acid composition modulates postprandial lipemia, but information on the other metabolic risk markers is limited. We therefore studied the acute effects of a meal rich in SFA compared with those of a meal rich in (n-6) PUFA on postprandial responses in overweight men who are at an increased risk to develop the metabolic syndrome and its comorbidities. In a crossover design, the effects of 50 g butter (rich in SFA) on lipemia and markers for inflammation and endothelial activity were compared with those of 50 g sunflower oil [rich in (n-6) PUFA] during an 8-h postprandial mixed meal tolerance test in 13 overweight men. Postprandial changes in serum TG were comparable between the meals (P = 0.38), except for a reduction in the incremental area under the curve (P = 0.046) in the late postprandial phase after (n-6) PUFA (125 ± 96 mmol⋅min⋅L(-1)) compared with SFA (148 ± 98 mmol⋅min⋅L(-1)). Compared with the SFA meal, the (n-6) PUFA meal decreased plasma IL-6 (P = 0.003), TNFα (P = 0.005), soluble TNF receptors I and II (sTNFr; P = 0.024 and P < 0.001, respectively), and soluble vascular cell adhesion molecule-1 (sVCAM-1; P = 0.030) concentrations. These results indicate that exchanging SFA from butterfat for (n-6) PUFA in a mixed meal may decrease postprandial lipemia and concentrations of IL-6, TNFα, sTNFr-I and -II, and sVCAM-1 in overweight men.
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Long-term efficacy and safety of ezetimibe/simvastatin coadministered with extended-release niacin in hyperlipidaemic patients with diabetes or metabolic syndrome.
Fazio, S, Guyton, JR, Lin, J, Tomassini, JE, Shah, A, Tershakovec, AM
Diabetes, obesity & metabolism. 2010;(11):983-93
Abstract
AIMS: To assess the efficacy and safety of ezetimibe/simvastatin (E/S) plus extended-release niacin (N) in hyperlipidaemic patients with diabetes mellitus (DM), metabolic syndrome (MetS) without DM (MetS/non-DM) or neither (non-DM/non-MetS). METHODS A subgroup analysis of a double-blind, 64-week trial of 1220 randomized patients who received E/S (10/20 mg) + N (to 2 g) or E/S (10/20 mg) for 64 weeks, or N (to 2 g) for 24 weeks then E/S (10/20 mg) + N (2 g) or E/S (10/20 mg) for 40 additional weeks. The evaluable populations of this analysis included n = 765 patients at 24 weeks and n = 574 at 64 weeks. Among those receiving N, only those who attained the 2-g dose were included in the analysis. RESULTS E/S+N improved levels of low-density lipoprotein cholesterol, other lipids and lipoprotein ratios compared with N and E/S at 24 weeks and E/S at 64 weeks. The combination increased high-density lipoprotein cholesterol and apolipoprotein AI comparably to N and more than E/S. E/S+N reduced high-sensitivity C-reactive protein (hsCRP) levels more effectively than N and similarly to E/S. E/S+N was generally well tolerated. Discontinuations due to flushing with N and E/S+N were comparable and greater than E/S in all subgroups. Fasting glucose trended higher for N vs. E/S. Glucose elevations from baseline to 12 weeks were highest for patients with DM (24.9 mg/dl for N, 21.2 mg/dl for E/S+N, 17.5 mg/dl for E/S); fasting glucose then declined to pretreatment levels at 64 weeks in all subgroups. New-onset DM was more frequent among MetS patients than those without MetS during the first 24 weeks and trended higher among those assigned to N-containing regimens [n = 5(5.1%) for N, n = 2(1.7%) for E/S, n = 21(8.8%) for E/S+N]; during the 24-64 week extension study, diabetes was diagnosed in five additional patients in the E/S(cumulative incidence of 5.9%) and one in the E/S+N (cumulative incidence of 9.2%). Treatment-incident elevations in uric acid levels were increased among subjects assigned to N-containing regimens, but there were no effects on symptomatic gout. CONCLUSION Combination E/S+N is a safe treatment option for hyperlipidaemic patients including those with DM and MetS, but requires monitoring of glucose and potentially uric acid levels.