scholarly journals Production of Structured Lipids Rich in Triacylglycerols Containing Medium-Chain Fatty Acids and Unsaturated Fatty Acids at the Sn-2 Position through Enzymatic Interesterification

Author(s):  
Siti Nurhasanah ◽  
Nur Wulandari ◽  
S Joni Munarso ◽  
Purwiyatno Hariyadi
2017 ◽  
Vol 82 (8) ◽  
pp. 1968-1977 ◽  
Author(s):  
Shengmin Zhou ◽  
Yueqiang Wang ◽  
Yuanrong Jiang ◽  
Zhongfei Zhang ◽  
Xiangjun Sun ◽  
...  

1987 ◽  
Vol 65 (12) ◽  
pp. 2459-2465 ◽  
Author(s):  
A. B. R. Thomson ◽  
M. Keelan ◽  
M. Garg ◽  
M. T. Clandinin

Isocaloric modification in the ratio of dietary polyunsaturated-to-saturated fatty acids influences intestinal uptake of actively and passively transported nutrients. This study was undertaken to determine which dietary fatty acid was responsible for these alterations in absorption. Adult female rats were fed isocaloric semisynthetic diets high in palmitic and stearic acids (SFA), oleic acid (OA), linoleic acid (LA), or linolenic acid (LNA). An in vitro technique was used to measure the uptake of varying concentrations of glucose as well as a series of fatty acids and cholesterol. Jejunal uptake of 40 mM glucose was highest in rats fed SFA and lowest in those fed LA; ileal glucose uptake was similar in OA, LA, and LNA, but was lowest in SFA. Jejunal uptake of medium-chain fatty acids (8:0–12:0) was higher in OA than in other diet groups; ileal uptake of medium-chain fatty acids was unaffected by diet. Jejunal and ileal uptake of 18:2 was higher in LNA than in SFA or OA; the uptake of the other long-chain saturated or unsaturated fatty acids was unchanged by diet. The ileal but not the jejunal uptake of cholesterol was increased in LA as compared with SFA or OA, and reduced in LNA as compared with LA. These transport changes were not explained by differences in the animals' food consumption, body weight gain, intestinal mass, or mucosal surface area. We postulate that these diet-induced transport alterations may be mediated via changes in brush border membrane phospholipid fatty acyl composition. Thus, intestinal transport of nutrients may be varied by isocaloric changes in the dietary content of individual fatty acids.


2009 ◽  
Vol 60 (2) ◽  
pp. 168-176 ◽  
Author(s):  
Maria M. C. Feltes ◽  
L. De Oliveira Pitol ◽  
J. F. Gomes Correia ◽  
R. Grimaldi ◽  
J. Mara Block ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1737
Author(s):  
Alexander Folwaczny ◽  
Elisa Waldmann ◽  
Julia Altenhofer ◽  
Kerstin Henze ◽  
Klaus G. Parhofer

Fasting and postprandial hypertriglyceridemia are causal risk factors for atherosclerosis. The prevalence of hypertriglyceridemia is approximately 25–30% and most hypertriglyceridemic patients suffer from mild to moderate hypertriglyceridemia. Data regarding dietary interventions on postprandial triglyceride metabolism of mildly to moderately hypertriglyceridemic patients is, however, sparse. In a randomized controlled trial, eight mildly hypertriglyceridemic patients and five healthy, normolipidemic controls received three separate standardized fat-meals containing either saturated fatty acids (SFA), mono-unsaturated fatty acids (MUFA), or medium-chain fatty acids (MCFA) in a randomized order. Fasting and postprandial lipid parameters were determined over a 10 h period and the (incremental) area under the curve (AUC/iAUC) for plasma triglycerides and other parameters were determined. MCFA do not lead to a significant elevation of postprandial total plasma triglycerides and other triglyceride parameters, while both SFA (patients: p = 0.003, controls: p = 0.03 compared to MCFA) and MUFA (patients: p = 0.001; controls: p = 0.14 compared to MCFA) do lead to such an increase. Patients experienced a significantly more pronounced increase of plasma triglycerides than controls (SFA: patients iAUC = 1006 mg*h/dL, controls iAUC = 247 mg*h/dL, p = 0.02; MUFA: patients iAUC = 962 mg*h/dL, controls iAUC = 248 mg*h/dL, p = 0.05). Replacing SFA with MCFA may be a treatment option for mildly to moderately hypertriglyceridemic patients as it prevents postprandial hypertriglyceridemia.


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