**1. Introduction**

288 Lipoproteins – Role in Health and Diseases

[110] Eilertsen KE. Manuscript in preparation.

Pharmacology. 2010;53(3-4):177-184.

rabbits. Atherosclerosis. 2002;163(1):79-87.

[111] Murakami S, Sakurai T, Toda Y, Morito A, Sakono M, Fukuda N. Prevention of neointima formation by taurine ingestion after carotid balloon injury. Vascular

[112] Murakami S, Kondo Y, Sakurai T, Kitajima H, Nagate T. Taurine suppresses development of atherosclerosis in Watanabe heritable hyperlipidemic (WHHL)

> For a long time, obesity has been known as a risk factor for cardiovascular disease, which is one of the main causes of death in developed countries. The prevalence of obesity (defined as having a body mass index [BMI] of 30 kg/m2 or more) is increasing in both developing and developed countries. A 5-kg/m2 increase in body mass index (BMI) increases the risk of cardiac complications by 29% [1]. This risk is due to the coexistence of other factors associated with obesity, such as hypertension, dyslipidemia, nonalcoholic fatty liver disease and abnormalities in glycemic metabolism. Resistances to insulin and lipid abnormalities are commonly found among obese patients with type 2 diabetes mellitus (T2DM) and are strongly related to an increase of cardiovascular risk. Resistance to insulin and consequent compensatory hyperinsulinemia significantly increase the risk of death due to cardiovascular diseases [2–5].

> To identify the patients with metabolic syndrome, insulin resistance, and greater cardiovascular risk, there are criteria, established by the Adult Treatment Panel III (NCEP ATP III), that include the presence of three of more of the following: central obesity (abdominal circumference above 102 cm in men and 88 cm in women), increased triglycerides (greater than or equal to 150 mg/dl) or use of a lipid-lowering agent, reduced HDL cholesterol (lower than 40 mg/dl among men and lower than 50mg/dl among women) or use of a lipid lowering agent, hypertension (systolic arterial pressure greater than or equal to 130 mmHg or diastolic pressure greater than or equal to 90mmHg) or use of an antihypertensive agent, andglucose levels greater than or equal to 100 mg/dl or use of an oral hypoglycemic agent and/or insulin [6].

> Despite this, recent studies propose that the use of the TG/HDL (Triglicerides/High Density Lipoprotein) ratio may be a more practical way to estimate insulin resistance. It is believed that the greater the ratio, the greater the insulin resistance of the patient. This ratio provides an estimate of the sensitivity to insulin and is as accurate as the criteria for the metabolic

© 2012 de Moura et al., licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2012 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

syndrome defined by the ATP III, the concentration of plasma insulin when fasting, or other estimates that measure the amount of glucose and the plasma concentration of insulin in order to evaluate its action [5, 7 -9]. Some studies suggest that the increase of the TG/HDL ratio may better predict the risk of cardiovascular diseases than do conventional risk factors such as hypertension, tobacco use, and physical activity [10].

To control the obesity and insulin resistance the initial steps are lifestyle changes aimed at controlling diet and increasing activity with the goal of reducing body weight, followed by the addition of orally active pharmacologic agents and insulin to the treatment regimen.

However, dietary modification and pharmaceutical therapy offer limited potential for sustained weight loss, effective in fewer than 5% of cases [2]. In a meta-analysis of pharmacotherapy for obesity, the percentages of patients achieving 5% and 10% weight loss thresholds by using anti obesity drugs were 54% and 18%, respectively, but a lack of adherence to treatment limited the efficacy and effectiveness [11].

Weight loss surgery, in contrast, has been shown to effect a more durable response . In addition, it can induce reversal of obesity-associated comorbidities [2,12].

Of interest is the observation that obese patients with diabetes who undergo certain gastric bypass procedures demonstrate improvement in glycemia, often within days of surgery and before significant weight loss. The exact mechanism responsible for this dramatic effect of surgical procedures for obesity on diabetes improvement is not fully understood; however, the surgical rearrangement of the anatomy of the gastrointestinal (GI) tract changes the location where partially digested nutrients first contact the intestine, suggesting that correction of dysfunctional homeostatic mechanisms may contribute to the glycemic improvement. Whether it is a pure effect of weight reduction or bypass of the hormonally active foregut has a primary effect remains a controversy. Hypothesis includes weight reduction, decreased caloric intake, and bypass of the hormonally active foregut [12-14].

However, weight loss surgery is associated with complications such as anastomotic leak and ulcer presenting a mortality rate estimates range between 0.1 and 2.0% [2].

Endoscopic weight loss therapies may provide some of the benefits of weight loss surgery while being reversible, with a lower risk profile, and being available to patients who do not qualify for surgery or are poor candidates for surgery. Those endoscopic solutions for weight loss are also applicable as metabolic procedures to address comorbidities as type 2 diabetes, dyslipidemia and nonalcoholic fatty liver disease.

#### **2. Physiopathology of metabolic improvement after metabolic surgery**

Several studies have shown a significant diabetes improvement in obese patients who undergo certain gastric bypass procedures. The improvement of glycemia is observed, often within days of surgery and before significant weight loss. The mechanism responsible for this improvement is not fully understood; however, the surgical rearrangement of the anatomy of the gastrointestinal tract may contribute to the glycemic improvement. If the glicemic improvement is a pure effect of weight reduction or bypass of the hormonally active foregut has a primary effect remains a controversy. Hypothesis to explain those effects includes weight reduction, decreased caloric intake, and bypass of the hormonally active.foregut. [12-14]

290 Lipoproteins – Role in Health and Diseases

syndrome defined by the ATP III, the concentration of plasma insulin when fasting, or other estimates that measure the amount of glucose and the plasma concentration of insulin in order to evaluate its action [5, 7 -9]. Some studies suggest that the increase of the TG/HDL ratio may better predict the risk of cardiovascular diseases than do conventional risk factors

To control the obesity and insulin resistance the initial steps are lifestyle changes aimed at controlling diet and increasing activity with the goal of reducing body weight, followed by the addition of orally active pharmacologic agents and insulin to the treatment regimen.

However, dietary modification and pharmaceutical therapy offer limited potential for sustained weight loss, effective in fewer than 5% of cases [2]. In a meta-analysis of pharmacotherapy for obesity, the percentages of patients achieving 5% and 10% weight loss thresholds by using anti obesity drugs were 54% and 18%, respectively, but a lack of

Weight loss surgery, in contrast, has been shown to effect a more durable response . In

Of interest is the observation that obese patients with diabetes who undergo certain gastric bypass procedures demonstrate improvement in glycemia, often within days of surgery and before significant weight loss. The exact mechanism responsible for this dramatic effect of surgical procedures for obesity on diabetes improvement is not fully understood; however, the surgical rearrangement of the anatomy of the gastrointestinal (GI) tract changes the location where partially digested nutrients first contact the intestine, suggesting that correction of dysfunctional homeostatic mechanisms may contribute to the glycemic improvement. Whether it is a pure effect of weight reduction or bypass of the hormonally active foregut has a primary effect remains a controversy. Hypothesis includes weight reduction, decreased caloric intake, and bypass of the hormonally active foregut [12-14].

However, weight loss surgery is associated with complications such as anastomotic leak and

Endoscopic weight loss therapies may provide some of the benefits of weight loss surgery while being reversible, with a lower risk profile, and being available to patients who do not qualify for surgery or are poor candidates for surgery. Those endoscopic solutions for weight loss are also applicable as metabolic procedures to address comorbidities as type 2

**2. Physiopathology of metabolic improvement after metabolic surgery** 

Several studies have shown a significant diabetes improvement in obese patients who undergo certain gastric bypass procedures. The improvement of glycemia is observed, often within days of surgery and before significant weight loss. The mechanism responsible for this improvement is not fully understood; however, the surgical rearrangement of the

such as hypertension, tobacco use, and physical activity [10].

adherence to treatment limited the efficacy and effectiveness [11].

addition, it can induce reversal of obesity-associated comorbidities [2,12].

ulcer presenting a mortality rate estimates range between 0.1 and 2.0% [2].

diabetes, dyslipidemia and nonalcoholic fatty liver disease.

Two hypothesis have been proposed to explain the effect of duodenal jejunal bypass on type 2 diabetes. The "hindgut hypothesis" holds that diabetes control results from the expedited delivery of nutrient chyme to the distal intestine, enhancing a physiologic signal that improves glucose metabolism. A potential candidate mediator of this effect is glucagon-like peptide 1 (GLP-1). This incretin hormone is secreted by L cells of the distal bowel in response to intestinal nutrients. It stimulates insulin secretion and exerts proliferative and antiapoptotic effects on pancreatic *beta* cells.16 If proven true, the hindgut hypothesis would spur further research on methods to enhance signaling by GLP-1 (or other distal gut peptides) to treat type 2 diabetes [14-16]. An alternative hypothesis is that the effect of selected bariatric operations on diabetes depends on exclusion of the duodenum and proximal jejunum from the transit of nutrients, possibly preventing secretion of a putative signal that promotes insulin resistance and type 2 diabetes ("foregut hypothesis"). Although no obvious candidate molecules can be identified with current knowledge, if proven true, this hypothesis might open new avenues in the search for the cause and cures of diabetes [14,17,18].

Several reports supported that the duodeno jejunal exclusion (foregut hypothesis) owes to a direct effect of the bypass of the hormonally active foregut. Rubino and Marescaux showed in their study in animal model that bypassing a short segment of proximal intestine directly ameliorates type 2 diabetes, independently of effects on food intake, body weight, malabsorption, or nutrient delivery to the hindgut [14].

However,in previous studies, it was observed that a strict calorie restriction, as performed in the first weeks after bariatric surgery, could bring itself to a normalization of plasma glucose and insulin levels before body weight decrease [19,20].

Wei-Jei Lee in a study comparing the band (restrictive) with the gastric bypass (duodeno jejunal bypass), with a longer follow-up, showed that the gastric banding group had a similar improvement of insulin resistance to the bypass group while similar weight reduction was achieved. The gastric banding group had similar result at postoperative 6 months compared to the gastric bypass group at the first postoperative month. Also, 3 months to 1 year and 6 months to 2 years were compatible. Suggesting that for a longterm effect of resolution of insulin resistance, sustained weight reduction plays the key mechanism [12].

Improvement in the glycemic control, insulin resistance and metabolic syndrome after bariatric surgery is regulated by a complex mechanism and still there is no certainty whether it is a pure effect of calorie restriction and weight reduction or it is caused by the bypass of the hormonally active foregut .
