<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet href="/rss.css" type="text/css"?>
<rdf:RDF xmlns="http://purl.org/rss/1.0/"
    xmlns:cc="http://web.resource.org/cc/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:extra="http://www.w3.org/1999/xhtml"
    xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#">
    <channel rdf:about="http://www.nutritionandmetabolism.com/feeds/mostaccessed/journal?quantity=&amp;format=rss&amp;version=">
        <title>Nutrition &amp; Metabolism - Most accessed articles</title>
        <link>http://www.nutritionandmetabolism.com</link>
        <description>The most accessed research articles published by Nutrition &amp; Metabolism</description>
        <dc:date>2012-02-03T00:00:00Z</dc:date>
        <items>
            <rdf:Seq>
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/9/1/5" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/1/1/2" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/2/1/25" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/2/1/5" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/8/1/75" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/5/1/1" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/9/1/8" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/9/1/3" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/7/1/51" />
                                <rdf:li rdf:resource="http://www.nutritionandmetabolism.com/content/8/1/92" />
                            </rdf:Seq>
        </items>
                 <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </channel>
        <item rdf:about="http://www.nutritionandmetabolism.com/content/9/1/5">
        <title>Quality protein intake is inversely associated with abdominal fat</title>
        <description>Dietary protein intake and specifically the quality of the protein in the diet has become an area of recent interest. This study determined the relationship between the amount of quality protein, carbohydrate, and dietary fat consumed and the amount of times the ~10g essential amino acid (EAA) threshold was reached at a meal, with percent central abdominal fat (CAF). Quality protein was defined as the ratio of EAA to total dietary protein. Quality protein consumed in a 24-hour period and the amount of times reaching the EAA threshold per day was inversely related to percent CAF, but not for carbohydrate or dietary fat.  In conclusion, moderate to strong correlations between variables indicate that quality and distribution of protein may play an important role in regulating CAF, which is a strong independent marker for disease and mortality.</description>
        <link>http://www.nutritionandmetabolism.com/content/9/1/5</link>
                <dc:creator>Jeremy Loenneke</dc:creator>
                <dc:creator>Jacob Wilson</dc:creator>
                <dc:creator>Anssi Manninen</dc:creator>
                <dc:creator>Mandy Wray</dc:creator>
                <dc:creator>Jeremy Barnes</dc:creator>
                <dc:creator>Thomas Pujol</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2012, null:5</dc:source>
        <dc:date>2012-01-27T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-9-5</dc:identifier>
                                <prism:require>/content/figures/1743-7075-9-5-toc.gif</prism:require>
                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2012-01-27T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.nutritionandmetabolism.com/content/1/1/2">
        <title>Ketogenic diets and physical performance</title>
        <description>Impaired physical performance is a common but not obligate result of a low carbohydrate diet. Lessons from traditional Inuit culture indicate that time for adaptation, optimized sodium and potassium nutriture, and constraint of protein to 15&#8211;25 % of daily energy expenditure allow unimpaired endurance performance despite nutritional ketosis.</description>
        <link>http://www.nutritionandmetabolism.com/content/1/1/2</link>
                <dc:creator>Stephen Phinney</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2004, null:2</dc:source>
        <dc:date>2004-08-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-1-2</dc:identifier>
                                <prism:require>/content/figures/1743-7075-1-2-toc.gif</prism:require>
                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2004-08-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.nutritionandmetabolism.com/content/2/1/25">
        <title>Dietary protein intake and renal function</title>
        <description>Recent trends in weight loss diets have led to a substantial increase in protein intake by individuals. As a result, the safety of habitually consuming dietary protein in excess of recommended intakes has been questioned. In particular, there is concern that high protein intake may promote renal damage by chronically increasing glomerular pressure and hyperfiltration. There is, however, a serious question as to whether there is significant evidence to support this relationship in healthy individuals. In fact, some studies suggest that hyperfiltration, the purported mechanism for renal damage, is a normal adaptative mechanism that occurs in response to several physiological conditions. This paper reviews the available evidence that increased dietary protein intake is a health concern in terms of the potential to initiate or promote renal disease. While protein restriction may be appropriate for treatment of existing kidney disease, we find no significant evidence for a detrimental effect of high protein intakes on kidney function in healthy persons after centuries of a high protein Western diet.</description>
        <link>http://www.nutritionandmetabolism.com/content/2/1/25</link>
                <dc:creator>William Martin</dc:creator>
                <dc:creator>Lawrence Armstrong</dc:creator>
                <dc:creator>Nancy Rodriguez</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2005, null:25</dc:source>
        <dc:date>2005-09-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-2-25</dc:identifier>
                                <prism:require>/content/figures/1743-7075-2-25-toc.gif</prism:require>
                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>25</prism:startingPage>
        <prism:publicationDate>2005-09-20T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.nutritionandmetabolism.com/content/2/1/5">
        <title>Fructose, insulin resistance, and metabolic dyslipidemia</title>
        <description>Obesity and type 2 diabetes are occurring at epidemic rates in the United States and many parts of the world. The &quot;obesity epidemic&quot; appears to have emerged largely from changes in our diet and reduced physical activity. An important but not well-appreciated dietary change has been the substantial increase in the amount of dietary fructose consumption from high intake of sucrose and high fructose corn syrup, a common sweetener used in the food industry. A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism. These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed with high fructose feeding in both humans and animal models. Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic and intestinal overproduction of atherogenic lipoprotein particles. Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome. There is an urgent need for increased public awareness of the risks associated with high fructose consumption and greater efforts should be made to curb the supplementation of packaged foods with high fructose additives. The present review will discuss the trends in fructose consumption, the metabolic consequences of increased fructose intake, and the molecular mechanisms leading to fructose-induced lipogenesis, insulin resistance and metabolic dyslipidemia.</description>
        <link>http://www.nutritionandmetabolism.com/content/2/1/5</link>
                <dc:creator>Heather Basciano</dc:creator>
                <dc:creator>Lisa Federico</dc:creator>
                <dc:creator>Khosrow Adeli</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2005, null:5</dc:source>
        <dc:date>2005-02-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-2-5</dc:identifier>
                                <prism:require>/content/figures/1743-7075-2-5-toc.gif</prism:require>
                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2005-02-21T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.nutritionandmetabolism.com/content/8/1/75">
        <title>Is there a role for carbohydrate restriction in the treatment and prevention of cancer?</title>
        <description>Over the last years, evidence has accumulated suggesting that by systematically reducing the amount of dietary carbohydrates (CHOs) one could suppress, or at least delay, the emergence of cancer, and that proliferation of already existing tumor cells could be slowed down. This hypothesis is supported by the association between modern chronic diseases like the metabolic syndrome and the risk of developing or dying from cancer. CHOs or glucose, to which more complex carbohydrates are ultimately digested, can have direct and indirect effects on tumor cell proliferation: first, contrary to normal cells, most malignant cells depend on steady glucose availability in the blood for their energy and biomass generating demands and are not able to metabolize significant amounts of fatty acids or ketone bodies due to mitochondrial dysfunction. Second, high insulin and insulin-like growth factor (IGF)-1 levels resulting from chronic ingestion of CHO-rich Western diet meals, can directly promote tumor cell proliferation via the insulin/IGF1 signaling pathway. Third, ketone bodies that are elevated when insulin and blood glucose levels are low, have been found to negatively affect proliferation of different malignant cells in vitro or not to be usable by tumor cells for metabolic demands, and a multitude of mouse models have shown anti-tumorigenic properties of very low CHO ketogenic diets. In addition, many cancer patients exhibit an altered glucose metabolism characterized by insulin resistance and may profit from an increased protein and fat intake.In this review, we address the possible beneficial effects of low CHO diets on cancer prevention and treatment. Emphasis will be placed on the role of insulin and IGF1 signaling in tumorigenesis as well as altered dietary needs of cancer patients.</description>
        <link>http://www.nutritionandmetabolism.com/content/8/1/75</link>
                <dc:creator>Rainer Klement</dc:creator>
                <dc:creator>Ulrike Kammerer</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2011, null:75</dc:source>
        <dc:date>2011-10-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-8-75</dc:identifier>
                                <prism:require>/content/figures/1743-7075-8-75-toc.gif</prism:require>
                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>75</prism:startingPage>
        <prism:publicationDate>2011-10-26T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.nutritionandmetabolism.com/content/5/1/1">
        <title>Effects of beta-hydroxy-beta-methylbutyrate (HMB) on exercise performance and body composition across varying levels of age, sex, and training experience: A review</title>
        <description>The leucine metabolite beta-hydroxy-beta-methylbutyrate (HMB) has been extensively used as an ergogenic aid; particularly among bodybuilders and strength/power athletes, who use it to promote exercise performance and skeletal muscle hypertrophy. While numerous studies have supported the efficacy of HMB in exercise and clinical conditions, there have been a number of conflicting results. Therefore, the first purpose of this paper will be to provide an in depth and objective analysis of HMB research. Special care is taken to present critical details of each study in an attempt to both examine the effectiveness of HMB as well as explain possible reasons for conflicting results seen in the literature. Within this analysis, moderator variables such as age, training experience, various states of muscle catabolism, and optimal dosages of HMB are discussed. The validity of dependent measurements, clustering of data, and a conflict of interest bias will also be analyzed. A second purpose of this paper is to provide a comprehensive discussion on possible mechanisms, which HMB may operate through. Currently, the most readily discussed mechanism has been attributed to HMB as a precursor to the rate limiting enzyme to cholesterol synthesis HMG-coenzyme A reductase. However, an increase in research has been directed towards possible proteolytic pathways HMB may operate through. Evidence from cachectic cancer studies suggests that HMB may inhibit the ubiquitin-proteasome proteolytic pathway responsible for the specific degradation of intracellular proteins. HMB may also directly stimulate protein synthesis, through an mTOR dependent mechanism. Finally, special care has been taken to provide future research implications.</description>
        <link>http://www.nutritionandmetabolism.com/content/5/1/1</link>
                <dc:creator>Gabriel Wilson</dc:creator>
                <dc:creator>Jacob Wilson</dc:creator>
                <dc:creator>Anssi Manninen</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2008, null:1</dc:source>
        <dc:date>2008-01-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-5-1</dc:identifier>
                                <prism:require>/content/figures/1743-7075-5-1-toc.gif</prism:require>
                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>1</prism:startingPage>
        <prism:publicationDate>2008-01-03T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.nutritionandmetabolism.com/content/9/1/8">
        <title>Flaxseed dietary fibers lower cholesterol and increase fecal fat excretion, but magnitude of effect depend on food type </title>
        <description>Background:
Dietary fibers have been proposed to play a role in cardiovascular risk as well as body weight management. Flaxseeds are a good source of dietary fibers, and a large proportion of these are water-soluble viscous fibers.MethodHere, we examine the effect of flaxseed dietary fibers in different food matrices on blood lipids and fecal excretion of fat and energy in a double-blind randomized crossover study with 17 subjects. Three different 7-d diets were tested: a low-fiber control diet (Control), a diet with flaxseed fiber drink (3/day) (Flax drink), and a diet with flaxseed fiber bread (3/day) (Flax bread). Total fat and energy excretion was measured in feces, blood samples were collected before and after each period, and appetite sensation registered 3 times daily before main meals.
Results:
Compared to control, Flax drink lowered fasting total-cholesterol and LDL-cholesterol by 12 and 15%, respectively, (p&lt;0.01), whereas Flax bread only produced a reduction of 7 and 9%, respectively (p&lt;0.05). Fecal fat and energy excretion increased by 50 and 23% with Flax drink consumption compared to control (p&lt;0.05), but only fecal fat excretion was increased with Flax bread compared to control (p&lt;0.05).
Conclusion:
Both Flax drink and Flax bread resulted in decreased plasma total and LDL-cholesterol and increased fat excretion, but the food matrix and/or processing may be of importance. Viscous flaxseed dietary fibers may be a useful tool for lowering blood cholesterol and potentially play a role in energy balance.Trial registration: The study was registered in the clinicaltrials.gov database: NCT00953004.</description>
        <link>http://www.nutritionandmetabolism.com/content/9/1/8</link>
                <dc:creator>Mette Kristensen</dc:creator>
                <dc:creator>Morten Jensen</dc:creator>
                <dc:creator>Julie Aarestrup</dc:creator>
                <dc:creator>Kristina Petersen</dc:creator>
                <dc:creator>Lise Sondergaard</dc:creator>
                <dc:creator>Mette Mikkelsen</dc:creator>
                <dc:creator>Arne Astrup</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2012, null:8</dc:source>
        <dc:date>2012-02-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-9-8</dc:identifier>
                                <prism:require>/content/figures/1743-7075-9-8-toc.gif</prism:require>
                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>8</prism:startingPage>
        <prism:publicationDate>2012-02-03T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.nutritionandmetabolism.com/content/9/1/3">
        <title>A high calcium diet containing nonfat dry milk reduces weight gain and associated adipose tissue inflammation in diet-induced obese mice when compared to high calcium alone</title>
        <description>Background:
High dietary calcium (Ca) is reported to have anti-obesity and anti-inflammatory properties.  Evidence for these properties of dietary Ca in animal models of polygenic obesity have been confounded by the inclusion of dairy food components in experimental diets; thus, effect of Ca per se could not be deciphered.  Furthermore, potential anti-inflammatory actions of Ca in vivo could not be dissociated from reduced adiposity.  Methods: We characterized adiposity along with metabolic and inflammatory phenotypes in diet-induced obese (DIO) mice fed 1 of 3 high fat diets (45% energy) for 12 wk: control (n = 29), high-Ca (n = 30), or high-Ca + nonfat dry milk (NFDM) (n = 30).  Results: Mice fed high-Ca + NFDM had reduced body weight and adiposity compared to high-Ca mice (P &lt; 0.001).  Surprisingly, the high-Ca mice had increased adiposity compared to lower-Ca controls (P &lt; 0.001).  Hyperphagia and increased feed efficiency contributed to obesity development in high-Ca mice, in contrast to NFDM mice that displayed significantly reduced weight gain despite higher energy intake compared to controls (P&lt;0.001).  mRNA markers of macrophages (e.g., CD68, CD11d) strongly correlated with body weight in all diet treatment groups, and most treatment differences in WAT inflammatory factor mRNA abundances were lost when controlling for body weight gain as a covariate.  Conclusions: The results indicate that high dietary Ca is not sufficient to dampen obesity-related phenotypes in DIO mice, and in fact exacerbates weight gain and hyperphagia.  The data further suggest that putative anti-obesity properties of dairy emanate from food components beyond Ca.</description>
        <link>http://www.nutritionandmetabolism.com/content/9/1/3</link>
                <dc:creator>Anthony Thomas</dc:creator>
                <dc:creator>Tamara Dunn</dc:creator>
                <dc:creator>Josephine Drayton</dc:creator>
                <dc:creator>Pieter Oort</dc:creator>
                <dc:creator>Sean Adams</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2012, null:3</dc:source>
        <dc:date>2012-01-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-9-3</dc:identifier>
                                <prism:require>/content/figures/1743-7075-9-3-toc.gif</prism:require>
                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2012-01-23T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.nutritionandmetabolism.com/content/7/1/51">
        <title>Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: A case for whey protein</title>
        <description>Regardless of age or gender, resistance training or provision of adequate amounts of dietary protein (PRO) or essential amino acids (EAA) can increase muscle protein synthesis (MPS) in healthy adults. Combined PRO or EAA ingestion proximal to resistance training, however, can augment the post-exercise MPS response and has been shown to elicit a greater anabolic effect than exercise plus carbohydrate. Unfortunately, chronic/adaptive response data comparing the effects of different protein sources is limited. A growing body of evidence does, however, suggest that dairy PRO, and whey in particular may: 1) stimulate the greatest rise in MPS, 2) result in greater muscle cross-sectional area when combined with chronic resistance training, and 3) at least in younger individuals, enhance exercise recovery. Therefore, this review will focus on whey protein supplementation and its effects on skeletal muscle mass when combined with heavy resistance training.</description>
        <link>http://www.nutritionandmetabolism.com/content/7/1/51</link>
                <dc:creator>Juha Hulmi</dc:creator>
                <dc:creator>Christopher Lockwood</dc:creator>
                <dc:creator>Jeffrey Stout</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2010, null:51</dc:source>
        <dc:date>2010-06-17T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-7-51</dc:identifier>
                                <prism:require>/content/figures/1743-7075-7-51-toc.gif</prism:require>
                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>51</prism:startingPage>
        <prism:publicationDate>2010-06-17T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.nutritionandmetabolism.com/content/8/1/92">
        <title>Carbohydrate restricted diet in conjunction with metformin and liraglutide is an effective treatment  in patients with deteriorated type 2 diabetes mellitus: Proof-of-concept study</title>
        <description>Background:
Type 2 diabetes mellitus is a chronic progressive disease. During the course of the disease intensive treatment is often necessary resulting in multiple interventions including administration of insulin. Although dietary intervention is highly recommended, the clinical results of the widely prescribed diets with low fat content and high carbohydrates are disappointing. In this proof-of-concept study, we tested the effect of dietary carbohydrate-restriction in conjunction with metformin and liraglutide on metabolic control in patients with type 2 diabetes.
Methods:
Forty patients with type 2 diabetes already being treated with two oral anti-diabetic drugs or insulin treatment and who showed deterioration of their glucose metabolism (i.e. HbA1c &gt; 7.5), were treated. A carbohydrate-restricted diet and a combination of metformin and liraglutide were instituted, after stopping either insulin or oral anti-diabetic drugs (excluding metformin). After enrollment, the study patients were scheduled for follow-up visits at one, two, three and six months. Primary outcome was glycemic control, measured by HbA1c at six months. Secondary outcomes were body weight, lipid-profile and treatment satisfaction.
Results:
Thirty-five (88 %) participants completed the study. Nearly all participating patients experienced a drop in HbA1c and body weight during the first three months, an effect which was maintained until the end of the study at six months. Seventy-one percent of the patients reached HbA1c values below 7.0 %. The range of body weight at enrollment was extreme, reaching 165 kg as the highest initial value. The average weight loss after 6 months was 10 %. Most patients were satisfied with this treatment. During the intervention no significant change of lipids was observed. Most patients who were on insulin could maintain the treatment without insulin with far better metabolic control.
Conclusions:
Carbohydrate restriction in conjunction with metformin and liraglutide is an effective treatment option for patients with advanced diabetes who are candidates for instituting insulin or who are in need of intensified insulin treatment. This proof-of-principle study showed a significant treatment effect on metabolic control.</description>
        <link>http://www.nutritionandmetabolism.com/content/8/1/92</link>
                <dc:creator>Juergen Mueller</dc:creator>
                <dc:creator>Dagmar Straeter-Mueller</dc:creator>
                <dc:creator>Hans-Joachim Marks</dc:creator>
                <dc:creator>Michael Glaesner</dc:creator>
                <dc:creator>Philipp Kneppe</dc:creator>
                <dc:creator>Beate Clemens-Harmening</dc:creator>
                <dc:creator>Harald Menker</dc:creator>
                <dc:source>Nutrition &amp; Metabolism 2011, null:92</dc:source>
        <dc:date>2011-12-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1743-7075-8-92</dc:identifier>
                                <prism:require>/content/figures/1743-7075-8-92-toc.gif</prism:require>
                <prism:publicationName>Nutrition &amp; Metabolism</prism:publicationName>
        <prism:issn>1743-7075</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>92</prism:startingPage>
        <prism:publicationDate>2011-12-23T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <cc:License rdf:about="http://creativecommons.org/licenses/by/2.0/">
        <cc:permits rdf:resource="http://creativecommons.org/ns#Reproduction" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#Distribution" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#DerivativeWorks" />
    </cc:License>
</rdf:RDF>

