8/6/2019 Docosahexaenoic Acid Enriched Functional Foods

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Premature birth and docosahexaenoic acid enriched functional foods: The

Department of Food Science and Human Nutrition at Colorado State University has

received a 1.2 million $ grant from the US Department of Agriculture to study the

effect of essential fatty acids in the diet on premature delivery. In collaboration with

Denver Health Hospital, this project will examine how diet fatty acids affect

premature delivery in 1200 pregnant women in the Denver area over a four year

period. Pregnant women who enroll in this study will be given a nutritional bar

containing various amounts of the nutritionally important fatty acid called

docosahexaenoic acid (DHA). The nutritional bar is being provided by OmegaTech,

Boulder Colorado, a company which is a leader in developing foods and food

products with increased DHA content. The study will determine what level of DHA is

needed to prevent premature delivery and how DHA affects prostaglandin

hormones that are important in pregnancy and delivery. Premature delivery occurs

in about 300,000 births annually in the US and accounts for several billion dollars in

health care costs. Premature delivery is an especially important problem in

Colorado which has one of the highest rates in the US, and preventing premature

delivery will improve infant weight at birth, and reduce the serious health problems

of the premature baby by increasing pregnancy duration. Obesity and Hepatic

Steatosis: Steatosis, is the earliest and most prevalent stage of non-alcoholic fatty

liver disease. Although steatosis generally has a benign outcome, some individuals

develop progressive liver injury (steatohepatitis or NASH). A large majority of

obese patients have hepatic steatosis and ~30% have NASH. The specific aim of

this project is to elucidate how saturated fatty acids in the steatotic liver lead to

increased liver cell injury. NIH funded. Nutrient Effects on Insulin Action: Organisms

reprogram metabolic pathways to adapt to changes in nutrient availability,

hormonal milieu and energy demands. This requires that stimuli are sensed and

highly specific responses engaged. We propose that in the liver, the mitogen-

activated protein kinase, c-Jun N-terminal kinase (JNK), links excessive nutrient

metabolism with impaired insulin regulation of glucose production. This aims of this

project are to a) determine the cellular effectors of fructose-induced activation of

JNK and insulin resistance and b) examine the role and regulation of the JNK

signaling module in fructose-induced insulin resistance. The results from these

studies will provide novel insight into nutrient regulation of signaling networks

within the hepatocyte and to the etiology of metabolic diseases, such as obesity

and type 2 diabetes, that have environmentally-based etiologies and are

characterized by hepatic insulin resistance. NIH funded.