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Evidence for multiple sites of insulin resistance. Guilherme, A. Adipocyte dysfunctions linking obesity to insulin resistance and type 2 diabetes. Cell Biol. Gerich, J. Renal gluconeogenesis: its importance in human glucose homeostasis. Diabetes Care 24 , — Honka, H. Validation of [ 18 F]fluorodeoxyglucose and positron emission tomography PET for the measurement of intestinal metabolism in pigs, and evidence of intestinal insulin resistance in patients with morbid obesity.

Diabetologia 56 , — Meijer, R. Insulin-induced microvascular recruitment in skin and muscle are related and both are associated with whole-body glucose uptake. Microcirculation 19 , — Insulin in the brain: its pathophysiological implications for states related with central insulin resistance, type 2 diabetes and Alzheimer’s disease.

Lausanne 5 , Kleinridders, A. Insulin action in brain regulates systemic metabolism and brain function. Kulkarni, R. Cell 96 , — Oliveira, J. Targeting type 2 diabetes: lessons from a knockout model of insulin receptor substrate 2. Samuel, V. Mechanisms for insulin resistance: common threads and missing links. Cell , — An excellent review of the molecular mechanism responsible for insulin resistance in T2DM and obesity.

Magnusson, I. Increased rate of gluconeogenesis in type II diabetes mellitus. A 13C nuclear magnetic resonance study.

This study demonstrated that increased rates of hepatic glucose production in patients with poorly controlled T2DM could entirely be attributed to increased rates of gluconeogenesis. Matsuda, M. Glucagon dose-response curve for hepatic glucose production and glucose disposal in type 2 diabetic patients and normal individuals.

Metabolism 51 , — Baron, A. Role of hyperglucagonemia in maintenance of increased rates of hepatic glucose output in type II diabetics. Diabetes 36 , — Influence of hyperinsulinemia, hyperglycemia, and the route of glucose administration on splanchnic glucose exchange.

USA 75 , — The disposal of an oral glucose load in patients with non-insulin-dependent diabetes. Metabolism 37 , 79—85 Characterization of renal glucose reabsorption in response to dapagliflozin in healthy subjects and subjects with type 2 diabetes. Barrett, E. Insulin regulates its own delivery to skeletal muscle by feed-forward actions on the vasculature.

Hemodynamic actions of insulin. Dissection of the insulin signaling pathway via quantitative phosphoproteomics. Cusi, K. Insulin resistance differentially affects the PI 3-kinase- and MAP kinase-mediated signaling in human muscle. Krook, A. Characterization of signal transduction and glucose transport in skeletal muscle from type 2 diabetic patients.

Diabetes 49 , — Copps, K. Diabetologia 55 , — Bouzakri, K. IRS-1 serine phosphorylation and insulin resistance in skeletal muscle from pancreas transplant recipients. Diabetes 55 , — Hiratani, K.

Krssak, M. Intramyocellular lipid concentrations are correlated with insulin sensitivity in humans: a 1H NMR spectroscopy study. Diabetologia 42 , — Petersen, K. Leptin reverses insulin resistance and hepatic steatosis in patients with severe lipodystrophy. Reversal of nonalcoholic hepatic steatosis, hepatic insulin resistance, and hyperglycemia by moderate weight reduction in patients with type 2 diabetes.

Lara-Castro, C. Intracellular lipid accumulation in liver and muscle and the insulin resistance syndrome. Yu, C. Mechanism by which fatty acids inhibit insulin activation of insulin receptor substrate-1 IRS-1 -associated phosphatidylinositol 3-kinase activity in muscle.

Bezy, O. Mechanism of hepatic insulin resistance in non-alcoholic fatty liver disease. Choi, C. Suppression of diacylglycerol acyltransferase-2 DGAT2 , but not DGAT1 , with antisense oligonucleotides reverses diet-induced hepatic steatosis and insulin resistance.

Morino, K. Reduced mitochondrial density and increased IRS-1 serine phosphorylation in muscle of insulin-resistant offspring of type 2 diabetic parents. Szendroedi, J. Larsen, P. On ceramides, other sphingolipids and impaired glucose homeostasis. Turpin, S. Obesity-induced CerS6-dependent C ceramide production promotes weight gain and glucose intolerance. Cantley, J. Patti, M. The role of mitochondria in the pathogenesis of type 2 diabetes. Mitochondrial dysfunction as a causative factor in the development of insulin resistance in T2DM is reviewed.

Ritov, V. Deficiency of subsarcolemmal mitochondria in obesity and type 2 diabetes. Diabetes 54 , 8—14 Mitochondrial dysfunction in the elderly: possible role in insulin resistance. Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes.

Mogensen, M. Mitochondrial respiration is decreased in skeletal muscle of patients with type 2 diabetes. Diabetes 56 , — Decreased insulin-stimulated ATP synthesis and phosphate transport in muscle of insulin-resistant offspring of type 2 diabetic parents.

Wang, C. Mitochondrial dysfunction leads to impairment of insulin sensitivity and adiponectin secretion in adipocytes. FEBS J. Rains, J. Oxidative stress, insulin signaling, and diabetes. Free Radic. Regulation of mitochondrial biogenesis by lipoprotein lipase in muscle of insulin-resistant offspring of parents with type 2 diabetes.

Diabetes 61 , — Romeo, G. Metabolic syndrome, insulin resistance, and roles of inflammation — mechanisms and therapeutic targets. Arkan, M. De Alvaro, C. Howard, J. Attenuation of leptin and insulin signaling by SOCS proteins.

Lebrun, P. SOCS proteins causing trouble in insulin action. Acta Physiol. Uysal, K. Endocrinology , — Ofei, F. Kim, J. Prevention of fat-induced insulin resistance by salicylate. Yuan, M. Goldfine, A. The effects of salsalate on glycemic control in patients with type 2 diabetes: a randomized trial.

Lumeng, C. Inflammatory links between obesity and metabolic disease. Nishimura, S. Feuerer, M. Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters. Bertola, A. Identification of adipose tissue dendritic cells correlated with obesity-associated insulin-resistance and inducing Th17 responses in mice and patients. Cai, D. Hepatic acetyl CoA links adipose tissue inflammation to hepatic insulin resistance and type 2 diabetes. Mori, M.

A systems biology approach identifies inflammatory abnormalities between mouse strains prior to development of metabolic disease. Diabetes 59 , — Mauer, J. Myeloid cell-restricted insulin receptor deficiency protects against obesity-induced inflammation and systemic insulin resistance. PLoS Genet. Shi, H. TLR4 links innate immunity and fatty acid-induced insulin resistance. Ron, D.

Signal integration in the endoplasmic reticulum unfolded protein response. Boden, G. Increase in endoplasmic reticulum stress-related proteins and genes in adipose tissue of obese, insulin-resistant individuals. Diabetes 57 , — Eizirik, D. The role for endoplasmic reticulum stress in diabetes mellitus. A comprehensive review of ER stress and the UPR in the development of insulin resistance and obesity.

Gregor, M. Endoplasmic reticulum stress is reduced in tissues of obese subjects after weight loss. Ozawa, K. The endoplasmic reticulum chaperone improves insulin resistance in type 2 diabetes. Herschkovitz, A. Common inhibitory serine sites phosphorylated by IRS-1 kinases, triggered by insulin and inducers of insulin resistance.

Sengupta, S. Regulation of the mTOR complex 1 pathway by nutrients, growth factors, and stress. Cell 40 , — Shah, O. Ozcan, U. Loss of the tuberous sclerosis complex tumor suppressors triggers the unfolded protein response to regulate insulin signaling and apoptosis. Cell 29 , — Park, S.

Stratton, I. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes UKPDS 35 : prospective observational study.

BMJ , — A seminal UK Prospective Diabetes Study study unequivocally demonstrating that improved glycaemic control reduced the incidence of microvascular, and to a lesser extent, macrovascular complications in patients with T2DM. Holman, R. Brownlee, M. The pathobiology of diabetic complications: a unifying mechanism.

A lucid discussion of the molecular pathways involved in the development of diabetic microvascular complications. Giacco, F. Oxidative stress and diabetic complications. Coutinho, M.

The relationship between glucose and incident cardiovascular events. A metaregression analysis of published data from 20 studies of 95, individuals followed for Diabetes Care 22 , — Taskinen, M.

New insights into the pathophysiology of dyslipidemia in type 2 diabetes. Atherosclerosis , — An up-to-date review of the pathogenesis of diabetic dyslipidaemia and its treatment.

Isomaa, B. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Adler, A. Association of systolic blood pressure with macrovascular and microvascular complications of type 2 diabetes UKPDS 36 : prospective observational study. Williams, B. Treating hypertension in patients with diabetes: when to start and how low to go? The optimal blood pressure goal in hypertensive patients with T2DM is discussed in light of the controversial results observed in the blood pressure arm of the ACCORD trial.

Lastra, G. Type 2 diabetes mellitus and hypertension: an update. International Expert Committee. International Expert Committee report on the role of the A1C assay in the diagnosis of diabetes. Diabetes Care 32 , — Diabetes Care 20 , — A reference publication by the ADA on the diagnosis and classification of diabetes mellitus.

Herman, W. Diabetes epidemiology: guiding clinical and public health practice: the Kelly West Award Lecture, A landmark lecture providing a comprehensive overview of the epidemiology of T2DM and the public health implications for diabetes prevention. Is the current definition for diabetes relevant to mortality risk from all causes and cardiovascular and noncardiovascular diseases? Diabetes Care 26 , — Engelgau, M. Screening for type 2 diabetes.

Diabetes Care 23 , — LeFevre, M. Behavioral counseling to promote a healthful diet and physical activity for cardiovascular disease prevention in adults with cardiovascular risk factors: U.

The diabetes risk score: a practical tool to predict type 2 diabetes risk. Tabaei, B. A multivariate logistic regression equation to screen for diabetes: development and validation. Diabetes Care 25 , — World Health Organization. Definition, diagnosis and classification of diabetes mellitus and its complications.

Part 1: diagnosis and classification of diabetes mellitus WHO, Pan, X. Knowler, W. Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. Ramachandran, A. Diabetologia 49 , — Chiasson, J. Kawamori, R. Voglibose for prevention of type 2 diabetes mellitus: a randomised, double-blind trial in Japanese individuals with impaired glucose tolerance. Prevention of type 2 diabetes with troglitazone in the Diabetes Prevention Program.

Effect of rosiglitazone on the frequency of diabetes in patients with impaired glucose tolerance or impaired fasting glucose: a randomised controlled trial. Li, G. The long-term effect of lifestyle interventions to prevent diabetes in the China Da Qing Diabetes Prevention Study: a year follow-up study. Sustained reduction in the incidence of type 2 diabetes by lifestyle intervention: follow-up of the Finnish Diabetes Prevention Study.

Pathophysiologic approach to therapy in patients with newly diagnosed type 2 diabetes. Diabetes Care 36 , S—S A rational approach to the treatment of T2DM is presented based on its pathophysiology. Raz, I. Nakagami, T. A year follow-up study. Lim, E. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol.

Jazet, I. Diabetologia 51 , — Initial combination therapy with metformin, pioglitazone and exenatide is more effective than sequential add-on therapy in subjects with new-onset diabetes. This prospective randomized trial using a combination of antidiabetic agents proven to reverse known pathophysiological abnormalities in T2DM demonstrated superiority of glycaemic control compared with the stepped approach of metformin followed by a sulfonylurea and then basal insulin recommended by most national diabetes organizations.

Harrison, L. Gram, J. Pharmacological treatment of the pathogenetic defects in type 2 diabetes: the randomized multicenter South Danish Diabetes Study. Diabetes Care 34 , 27—33 Combination of empagliflozin and linagliptin as second-line therapy in subjects with type 2 diabetes inadequately controlled on metformin. Diabetes Care 38 , — Weng, J. Hu, Y. One of several recent studies demonstrating that intensive insulin therapy to correct the decompensated metabolic state in newly diagnosed patients with T2DM can lead to durable glycaemic control without or with a marked reduction in antidiabetic medications.

Xiang, A. Astrup, A. Safety, tolerability and sustained weight loss over 2 years with the once-daily human GLP-1 analog, liraglutide. Metabolic effects of metformin on glucose and lactate metabolism in noninsulin-dependent diabetes mellitus.

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A 5-year ADOPT study demonstrating long-term durable HbA1c reduction with rosiglitazone compared with a progressive rise in HbA1c observed with metformin and sulfonylureas, and a more rapid deterioration of glycaemic control with sulfonylureas compared with metformin. Madiraju, A. Metformin suppresses gluconeogenesis by inhibiting mitochondrial glycerophosphate dehydrogenase.

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Solution to bridge existing care systems and apps on Google Cloud. Meta-analysis: the effect of dietary counseling for weight loss. Purcell, K. The effect of rate of weight loss on long-term weight management: a randomised controlled trial. Lancet Diabetes Endocrinol. Ali, M. How effective were lifestyle interventions in real-world settings that were modeled on the Diabetes Prevention Program?

Health Aff. Millwood 31 , 67—75 Tuomilehto, J. Prevention of type 2 diabetes mellitus by changes in lifestyle among subjects with impaired glucose tolerance.

Inzucchi, S. Diabetes Care 35 , — ADA position statement on the treatment of T2DM, advocating a stepped care approach starting with metformin. American Association of Clinical Endocrinologists. AACE position statement on the treatment of T2DM, advocating initial monotherapy or combination therapy based upon the starting HbA1c, and recommending various antidiabetic medications as initial therapy. Google Scholar. Pozzilli, P. Diabetes Metab. The first published report by key opinion leaders recommending individualized therapy based on the age and body weight of patients, the presence or absence of complications, and duration and aetiology of disease.

International Diabetes Federation. IDF [online] , Hu, F. Globalization of diabetes: the role of diet, lifestyle, and genes. Diabetes Care 34 , — An important study emphasizing the role of diet, physical activity and genes — beyond obesity — in the diabetes epidemic that is engulfing Asian countries as they are exposed to westernization.

Chan, J. Diabetes in Asia: epidemiology, risk factors, and pathophysiology. JAMA , — Ley, S. Prevention and management of type 2 diabetes: dietary components and nutritional strategies. A prospective study of weight training and risk of type 2 diabetes mellitus in men. Television viewing and risk of type 2 diabetes, cardiovascular disease, and all-cause mortality: a meta-analysis. Cappuccio, F. Quantity and quality of sleep and incidence of type 2 diabetes: a systematic review and meta-analysis.

Diabetes Care 33 , — Pan, A. Rotating night shift work and risk of type 2 diabetes: two prospective cohort studies in women. PLoS Med. Barnett, A. Diabetes in identical twins. A study of pairs. Diabetologia 20 , 87—93 Wang, Y. Wang, X. Inflammatory markers and risk of type 2 diabetes: a systematic review and meta-analysis. Li, S. Adiponectin levels and risk of type 2 diabetes: a systematic review and meta-analysis. Ding, E. Sex hormone-binding globulin and risk of type 2 diabetes in women and men.

Wang, T. Metabolite profiles and the risk of developing diabetes. Esteve, E. Gut microbiota interactions with obesity, insulin resistance and type 2 diabetes: did gut microbiote co-evolve with insulin resistance?

Care 14 , — Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. Schellenberg, E. Lifestyle interventions for patients with and at risk for type 2 diabetes.

A comprehensive review of the effectiveness of lifestyle intervention in the treatment of T2DM, emphasizing that, although initially successful, most subjects with diabetes regain the majority of lost weight over the subsequent 3—5 years. Insulin resistance, lipotoxicity, type 2 diabetes and atherosclerosis: the missing links. The Claude Bernard Lecture Diabetologia 53 , — Hemminki, K. Familial risks for type 2 diabetes in Sweden.

Groop, L. Diabetes 45 , — Lyssenko, V. Predictors of and longitudinal changes in insulin sensitivity and secretion preceding onset of type 2 diabetes. Diabetes 54 , — Grant, S. Variant of transcription factor 7-like 2 TCF7L2 gene confers risk of type 2 diabetes. Mechanisms by which common variants in the TCF7L2 gene increase risk of type 2 diabetes.

Sladek, R. A genome-wide association study identifies novel risk loci for type 2 diabetes. Nature , — Saxena, R. Genome-wide association analysis identifies loci for type 2 diabetes and triglyceride levels. Science , — Morris, A. Large-scale association analysis provides insights into the genetic architecture and pathophysiology of type 2 diabetes. Flannick, J. Loss-of-function mutations in SLC30A8 protect against type 2 diabetes.

Common variant in MTNR1B associated with increased risk of type 2 diabetes and impaired early insulin secretion. Rosengren, A. Overexpression of alpha2A-adrenergic receptors contributes to type 2 diabetes.

Tang, Y. Transl Med. These paper provides an example in which a genetic finding in an animal model of diabetes has been translated into a drug target in humans, the ADRA2A gene. De Jesus, D. Epigenetic modifiers of islet function and mass. Trends Endocrinol. Ozcan, S. Clinical risk factors, DNA variants, and the development of type 2 diabetes. This paper presents a genetic explanation for the development of T2DM. Travers, M. Insights into the molecular mechanism for type 2 diabetes susceptibility at the KCNQ1 locus from temporal changes in imprinting status in human islets.

Diabetes 62 , — Gulli, G. Diabetes 41 , — Martin, B. Role of glucose and insulin resistance in development of type 2 diabetes mellitus: results of a year follow-up study. Metabolism 63 , — Kahn, S. Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future. Muller, D. Insulin response during the oral glucose tolerance test: the role of age, sex, body fat and the pattern of fat distribution.

Aging Milano 8 , 13—21 CAS Google Scholar. Nauck, M. Secretion of glucagon-like peptide-1 GLP-1 in type 2 diabetes: what is up, what is down? Diabetologia 54 , 10—18 Madsbad, S. The role of glucagon-like peptide-1 impairment in obesity and potential therapeutic implications.

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Geffen realized that CDNow could link directly from the artist on its website to Geffen’s website, bypassing the CDNow home page and going directly to an artist’s music page. When visitors clicked on the associate’s website to go to Amazon and purchase a book, the associate received a commission. Amazon was not the first merchant to offer an affiliate program, but its program was the first to become widely known and serve as a model for subsequent programs.

In February , Amazon announced that it had been granted a patent [16] on components of an affiliate program. Affiliate marketing has grown quickly since its inception. The e-commerce website, viewed as a marketing toy in the early days of the Internet, became an integrated part of the overall business plan and in some cases grew to a bigger business than the existing offline business. In , the most active sectors for affiliate marketing were the adult gambling, retail industries and file-sharing services.

Also several of the affiliate solution providers expect to see increased interest from business-to-business marketers and advertisers in using affiliate marketing as part of their mix.

Websites and services based on Web 2. These platforms allow improved communication between merchants and affiliates. Web 2. Contextual ads allow publishers with lower levels of web traffic to place affiliate ads on websites.

Forms of new media have also diversified how companies, brands, and ad networks serve ads to visitors. For instance, YouTube allows video-makers to embed advertisements through Google’s affiliate network. Emerging black sheep are detected and made known to the affiliate marketing community with much greater speed and efficiency.

Eighty percent of affiliate programs today use revenue sharing or pay per sale PPS as a compensation method, nineteen percent use cost per action CPA , and the remaining programs use other methods such as cost per click CPC or cost per mille CPM, cost per estimated views.

Within more mature markets, less than one percent of traditional affiliate marketing programs today use cost per click and cost per mille. However, these compensation methods are used heavily in display advertising and paid search. Cost per mille requires only that the publisher make the advertising available on his or her website and display it to the page visitors in order to receive a commission. Pay per click requires one additional step in the conversion process to generate revenue for the publisher: A visitor must not only be made aware of the advertisement but must also click on the advertisement to visit the advertiser’s website.

Cost per click was more common in the early days of affiliate marketing but has diminished in use over time due to click fraud issues very similar to the click fraud issues modern search engines are facing today. Contextual advertising programs are not considered in the statistic pertaining to the diminished use of cost per click, as it is uncertain if contextual advertising can be considered affiliate marketing.

While these models have diminished in mature e-commerce and online advertising markets they are still prevalent in some more nascent industries. China is one example where Affiliate Marketing does not overtly resemble the same model in the West.

This leaves the greater, and, in case of cost per mille, the full risk and loss if the visitor cannot be converted to the advertiser. The advertiser must convert that visitor first. It is in the best interest of the affiliate to send the most closely targeted traffic to the advertiser as possible to increase the chance of a conversion.

The risk is absorbed by the affiliate who funnels their traffic to the campaign normally a landing page. In the case a conversion is not fired the publisher won’t receive any compensation for the traffic. Affiliate marketing is also called “performance marketing”, in reference to how sales employees are typically being compensated. Such employees are typically paid a commission for each sale they close, and sometimes are paid performance incentives for exceeding objectives.

The phrase, “Affiliates are an extended sales force for your business”, which is often used to explain affiliate marketing, is not completely accurate. The primary difference between the two is that affiliate marketers provide little if any influence on a possible prospect in the conversion process once that prospect is directed to the advertiser’s website.

The sales team of the advertiser, however, does have the control and influence up to the point where the prospect either a signs the contract, or b completes the purchase. Some advertisers offer multi-tier programs that distribute commission into a hierarchical referral network of sign-ups and sub-partners.

In practical terms, publisher “A” signs up to the program with an advertiser and gets rewarded for the agreed activity conducted by a referred visitor. If publisher “A” attracts publishers “B” and “C” to sign up for the same program using his sign-up code, all future activities performed by publishers “B” and “C” will result in additional commission at a lower rate for publisher “A”.

Two-tier programs exist in the minority of affiliate programs; most are simply one-tier. Merchants favor affiliate marketing because in most cases it uses a “pay for performance” model, meaning that the merchant does not incur a marketing expense unless results are accrued excluding any initial setup cost.