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postgraduate thesis: Maternal bitter melon supplementation reduces the risk for metabolic defects later in life: effects on lipidhandling, oxidative stress and inflammation in offspring born to damsfed a high fructose diet

TitleMaternal bitter melon supplementation reduces the risk for metabolic defects later in life: effects on lipidhandling, oxidative stress and inflammation in offspring born to damsfed a high fructose diet
Authors
Issue Date2012
PublisherThe University of Hong Kong (Pokfulam, Hong Kong)
Citation
Ching, H. [程曉霞]. (2012). Maternal bitter melon supplementation reduces the risk for metabolic defects later in life : effects on lipid handling, oxidative stress and inflammation in offspring born to dams fed a high fructose diet. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775255
AbstractThe relationship between fructose consumption and metabolic diseases has drawn substantial attention in recent years. Dietary fructose consumption has climbed dramatically in the past 40 years, and this trend coincides with the prevalence of obesity and diabetes worldwide. In rodents, maternal obesogenic diets are associated with higher risks of metabolic derangement later in life whereas bitter melon (BM) supplementation has been shown to improve blood glucose and lipid profiles. The overall objective of this thesis was to test the hypothesis that through developmental programming metabolic derangement in offspring born to rat dams fed a high-fructose (F) diet could be offset by the addition of BM to the maternal diet. Virgin female rats received a control (C), F (60%) or BM-supplemented F (FBM,1%) diet 8 weeks before conception and throughout gestation and lactation. Weaned male offspring consumed C diet (C/C,F/C,FBM/C) for 11 weeks. The concentrations of serum insulin, triglyceride, free fatty acid (FFA), and hepatic lipids in FBM/C offspring matched that in C/C offspring and were significantly lower than F/C offspring. These phenotypic changes were accompanied with suppressed hepatic lipogenic gene expression but enhanced expression of lipid oxidation-related genes. In the second experiment, we extended the earlier findings by examining whether adding BM to F-fed dams would still benefit offspring if they continued to consume the F diet postweaning. This simulates the scenario in affluent societies where fructose overconsumption may occur in two consecutive generations. The dose-response effect of BM at doses of 0.85% (FBM1) and 1% (FBM2) was also examined. Male offspring born to dams fed the C, F, FBM1 or FBM2 diet were weaned to C or F diet (C/C,C/F,F/F,FBM1/F,FBM2/F) for 20 weeks. BM normalized the serum FFA elevation observed in F/F offspring, although hyperinsulinemia remained in FBM1/F and FBM2/F offspring. The altered liver lipid profile and its molecular changes observed in F/F offspring were ameliorated by maternal BM supplementation. Lower adipose expression of mesoderm-specific transcript, hormone sensitive lipase, sterol regulatory element-binding transcription factor 1, and peroxisome proliferator-activated receptor-gamma (PPARγ) and PPARγ-target genes in FBM1/F and FBM2/F offspring indicated that BM could reduce adipocyte size as well as lower lipolysis and lipogenesis. Since FFA stimulates reactive oxygen species generation that enhances cellular stress, oxidative stress and inflammation in offspring of two-generation F exposure with or without maternal BM supplementation were examined. FBM1/F and FBM2/F offspring showed reduced lipid peroxidation but enhanced antioxidant capacity in the liver. BM suppressed the expression of proinflammatory genes and phosphorylation of c-Jun amino terminal kinase1, as well as promoted insulin receptor substrate 1 protein expression. These BM-mediated antioxidant and anti-inflammatory effects may be associated with a reduction of circulating FFA. Taken together, the data support the concept of developmental programming as maternal fructose clearly induced dyslipidemia, adipocyte dysfunction, oxidative stress and inflammation in offspring. That these abnormalities were largely reversed by adding BM to the maternal diet suggests that perinatal BFC supplementation could alter the course of maternal malnutrition-induced metabolic defects later in life.
DegreeDoctor of Philosophy
SubjectMetabolism - Disorders.
Momordica charantia - Therapeutic use.
Dept/ProgramBiological Sciences

 

DC FieldValueLanguage
dc.contributor.authorChing, Hiu-ha.-
dc.contributor.author程曉霞.-
dc.date.issued2012-
dc.identifier.citationChing, H. [程曉霞]. (2012). Maternal bitter melon supplementation reduces the risk for metabolic defects later in life : effects on lipid handling, oxidative stress and inflammation in offspring born to dams fed a high fructose diet. (Thesis). University of Hong Kong, Pokfulam, Hong Kong SAR. Retrieved from http://dx.doi.org/10.5353/th_b4775255-
dc.description.abstractThe relationship between fructose consumption and metabolic diseases has drawn substantial attention in recent years. Dietary fructose consumption has climbed dramatically in the past 40 years, and this trend coincides with the prevalence of obesity and diabetes worldwide. In rodents, maternal obesogenic diets are associated with higher risks of metabolic derangement later in life whereas bitter melon (BM) supplementation has been shown to improve blood glucose and lipid profiles. The overall objective of this thesis was to test the hypothesis that through developmental programming metabolic derangement in offspring born to rat dams fed a high-fructose (F) diet could be offset by the addition of BM to the maternal diet. Virgin female rats received a control (C), F (60%) or BM-supplemented F (FBM,1%) diet 8 weeks before conception and throughout gestation and lactation. Weaned male offspring consumed C diet (C/C,F/C,FBM/C) for 11 weeks. The concentrations of serum insulin, triglyceride, free fatty acid (FFA), and hepatic lipids in FBM/C offspring matched that in C/C offspring and were significantly lower than F/C offspring. These phenotypic changes were accompanied with suppressed hepatic lipogenic gene expression but enhanced expression of lipid oxidation-related genes. In the second experiment, we extended the earlier findings by examining whether adding BM to F-fed dams would still benefit offspring if they continued to consume the F diet postweaning. This simulates the scenario in affluent societies where fructose overconsumption may occur in two consecutive generations. The dose-response effect of BM at doses of 0.85% (FBM1) and 1% (FBM2) was also examined. Male offspring born to dams fed the C, F, FBM1 or FBM2 diet were weaned to C or F diet (C/C,C/F,F/F,FBM1/F,FBM2/F) for 20 weeks. BM normalized the serum FFA elevation observed in F/F offspring, although hyperinsulinemia remained in FBM1/F and FBM2/F offspring. The altered liver lipid profile and its molecular changes observed in F/F offspring were ameliorated by maternal BM supplementation. Lower adipose expression of mesoderm-specific transcript, hormone sensitive lipase, sterol regulatory element-binding transcription factor 1, and peroxisome proliferator-activated receptor-gamma (PPARγ) and PPARγ-target genes in FBM1/F and FBM2/F offspring indicated that BM could reduce adipocyte size as well as lower lipolysis and lipogenesis. Since FFA stimulates reactive oxygen species generation that enhances cellular stress, oxidative stress and inflammation in offspring of two-generation F exposure with or without maternal BM supplementation were examined. FBM1/F and FBM2/F offspring showed reduced lipid peroxidation but enhanced antioxidant capacity in the liver. BM suppressed the expression of proinflammatory genes and phosphorylation of c-Jun amino terminal kinase1, as well as promoted insulin receptor substrate 1 protein expression. These BM-mediated antioxidant and anti-inflammatory effects may be associated with a reduction of circulating FFA. Taken together, the data support the concept of developmental programming as maternal fructose clearly induced dyslipidemia, adipocyte dysfunction, oxidative stress and inflammation in offspring. That these abnormalities were largely reversed by adding BM to the maternal diet suggests that perinatal BFC supplementation could alter the course of maternal malnutrition-induced metabolic defects later in life.-
dc.languageeng-
dc.publisherThe University of Hong Kong (Pokfulam, Hong Kong)-
dc.relation.ispartofHKU Theses Online (HKUTO)-
dc.rightsThe author retains all proprietary rights, (such as patent rights) and the right to use in future works.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.source.urihttp://hub.hku.hk/bib/B47752555-
dc.subject.lcshMetabolism - Disorders.-
dc.subject.lcshMomordica charantia - Therapeutic use.-
dc.titleMaternal bitter melon supplementation reduces the risk for metabolic defects later in life: effects on lipidhandling, oxidative stress and inflammation in offspring born to damsfed a high fructose diet-
dc.typePG_Thesis-
dc.identifier.hkulb4775255-
dc.description.thesisnameDoctor of Philosophy-
dc.description.thesislevelDoctoral-
dc.description.thesisdisciplineBiological Sciences-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.5353/th_b4775255-
dc.date.hkucongregation2012-

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