New targets to treat obesity and the metabolic syndrome

Martin, Kathleen A.; Mani, Mitra; Mani, Arya

doi:10.1016/j.ejphar.2015.03.093

Cited by 102 publications

(71 citation statements)

References 185 publications

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“…This suggests that Dyrk1B may play an important role appetite regulation. NPY is also postulated to increase Dyrk1B expression via the PKA-CREB pathway, as Dyrk1B has a CREB motif in its promoter region [41]. …”

Section: Monogenic Causes Of Metabolic Syndromementioning

confidence: 99%

Metabolic syndrome

Ziki

Mani

2016

Current Opinion in Lipidology

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Purpose of review Metabolic syndrome (MetS) is a cluster of inter-related and heritable metabolic traits, which collectively impart unsurpassed risk for atherosclerotic cardiovascular disease and type 2 diabetes. Considerable work has been done to understand the underlying disease mechanisms by elucidating its genetic etiology. Recent findings Genome-wide association studies (GWAS) have been widely utilized albeit with modest success in identifying variants that are associated with more than two metabolic traits. Another limitation of this approach is the inherent small effect of the common variants, a major barrier for dissecting their cognate pathways. Modest advances in this venue have been also made by genetic studies of kindreds at the extreme ends of quantitative distributions. These efforts have led to the discovery of a number of disease genes with large effects that underlie the association of diverse traits of this syndrome. Summary Substantial progress has been made over the last decade in identification of genetic risk factors associated with the various traits of MetS. The heterogeneity and multifactorial heritability of MetS, however, has been a challenge towards understanding the factors underlying the association of these traits. Genetic investigations of outlier kindreds or homogenous populations with high prevalence for the disease can potentially improve our knowledge of the disease pathophysiology.

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Section: Monogenic Causes Of Metabolic Syndromementioning

confidence: 99%

Metabolic syndrome

Ziki

Mani

2016

Current Opinion in Lipidology

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“…PYY (3-36), the major circulating form, is produced by cleavage of the N-terminal TyrosineProline residues from PYY (1-36) by the enzyme dipeptidyl-peptidase-IV (DPP-IV) (Wynne et al 2005). Currently, the DPP-IV inhibitors are being evaluated for their eff ects on the obesity and metabolic traits (Martin et al 2015).…”

Section: Role Of the Gastrointestinal Tract Peptidesmentioning

confidence: 99%

Central and peripheral control of food intake

Abdalla

2017

Endocrine Regulations

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Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive. Th e body weight depends on the balance between the energy intake and energy expenditure. Increased food intake over the energy expenditure of prolonged time period results in an obesity. Th e obesity has become an important worldwide health problem, even at low levels. Th e obesity has an evil eff ect on the health and is associated with a shorter life expectancy. A complex of central and peripheral physiological signals is involved in the control of the food intake. Centrally, the food intake is controlled by the hypothalamus, the brainstem, and endocannabinoids and peripherally by the satiety and adiposity signals. Comprehension of the signals that control food intake and energy balance may open a new therapeutic approaches directed against the obesity and its associated complications, as is the insulin resistance and others. In conclusion, the present review summarizes the current knowledge about the complex system of the peripheral and central regulatory mechanisms of food intake and their potential therapeutic implications in the treatment of obesity. Th e maintenance of the body weight at a stable level is a major determinant in keeping the higher animals and mammals survive (Jequier and Tappy 1999). As a compensatory mechanism, hunger increases and energy expenditure decreases the weight loss. However, opposite responses are triggered when body weight increases. Body weight can change only when energy intake is not equal to energy expenditure over a given period of time (Bray et al. 2012). A complex physiological control system is involved in the maintenance of the energy balance. Th is system includes aff erent signals from the periphery about the state of the energy stores and eff erent signals that affect the energy intake and expenditure (Sandoval et al. 2008). Th is regulatory system is formed by multiple interactions between the gastrointestinal tract (GIT), adipose tissue, and the central nervous system (CNS). It is infl uenced by behavioral, sensorial, autonomic, nutritional, and endocrine mechanisms (Boguszewski et al. 2010). Satiety and adiposity signalsTh e food intake control includes a short-term regulation, which determines the beginning and the end of a meal (hunger and satiation) and the interval between the meals (satiety) and a long-term regulation with factors (signals of adiposity), which help to regulate the body energy depots (Cummings and Overduin 2007).Th e satiation means a suppression of the hunger and termination of the food intake aft er ingestion of Unauthenticated Download Date | 5/11/18 9:54 AM

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“…MetS is a specific set of metabolic traits which increase T2DM and CVD risk over any single CVD risk factor 1. While diet and exercise have had a dramatic impact at the individual level, they have done little to improve obesity and BMI at the population level 1…”

Section: Discussionmentioning

confidence: 99%

“…Obesity is a paramount 21st century health concern, wherein approximately 2 billion adults worldwide are either obese or overweight 1. The US Census Bureau reports that by 2050, the number of US adults aged 65 and over is expected to double, climbing from 40.2 million to 88.5 million 2.…”

Section: Introductionmentioning

confidence: 99%

Successful treatment of obesity and insulin resistance via ketogenic diet status post Roux-en-Y

Handley¹,

Bentley

Brown

et al. 2018

BMJ Case Reports

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This is a single case of a 65-year-old American woman who presented with substantial weight gain and insulin resistance (IR) post-Roux-en-Y gastric bypass (RYGB) surgery. Before RYGB, she had reached 340 lbs (155 kg) and a body mass index (BMI) of 56.6 kg/m The surgery resulted in a 70 lbs (32 kg) weight loss, bringing her BMI, per cent total weight loss (%TWL) and per cent excess weight loss (%EWL) to 44.9 kg/m, 20.6% and 36.8%, respectively. Unfortunately, her BMI would return to 53.6 kg/m, nearly her pre-RYGB BMI. It was then she sought the guidance of a primary care physician with expertise in nutrition and medical management of obesity, who placed her on a ketogenic diet. One year later, she had lost 102 lbs (46.4 kg), resulting in a BMI, %TWL and %EWL of 36.6 kg/m, 31.7%, and 63.1%, respectively, also further resulting in significant improvements of her inflammatory biomarkers. This case presentation will explore current literature, covering the effects of obesity on IR, pre-diabetes and other disease-provoking inflammatory biomarkers.

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New targets to treat obesity and the metabolic syndrome

Cited by 102 publications

References 185 publications

Metabolic syndrome

Metabolic syndrome

Central and peripheral control of food intake

Successful treatment of obesity and insulin resistance via ketogenic diet status post Roux-en-Y

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