Counterregulation of insulin by leptin as key component of autonomic regulation of body weight

Borer, Katarina T.

doi:10.4239/wjd.v5.i5.606

Cited by 32 publications

(24 citation statements)

References 332 publications

(444 reference statements)

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“…15 Another cause of inflammation is oxidative stress, which can be triggered by adipocytes. When fat mass increases, insufficient irrigation can lead to lack of oxygen and, thus, to cell necrosis.…”

Section: Metabolic Syndrome and Oxidative Stressmentioning

confidence: 99%

The role of oxidative stress on the pathophysiology of metabolic syndrome

Francisqueti

Chiaverini

Santos

et al. 2017

Rev. Assoc. Med. Bras.

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The role of oxidaTive sTress on The paThophysiology of meTabolic syndrome rev assoc Med Bras 2017; 63(1):85-91 85 REVIEW ARTICLEThe role of oxidative stress on the pathophysiology of metabolic syndrome Metabolic syndrome (MetS) has a high prevalence around the world. Considering the components used to classify MetS, it is clear that it is closely related to obesity. These two conditions begin with an increase in abdominal adipose tissue, which is metabolically more active, containing a greater amount of resident macrophages compared to other fat deposits. Abdominal adiposity promotes inflammation and oxidative stress, which are precursors of various complications involving MetS components, namely insulin resistance, hypertension and hyperlipidemia. One way to block the effects of oxidative stress would be through the antioxidant defense system, which offsets the excess free radicals. It is known that individuals with metabolic syndrome and obesity have high consumption of fats and sugars originated from processed foods containing high levels of sodium as well as low intake of fruits and vegetables, thus maintaining a state of oxidative stress, that can speed up the onset of MetS. Healthy eating habits could prevent or delay MetS by adding antioxidant-rich foods into the diet.

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Section: Metabolic Syndrome and Oxidative Stressmentioning

confidence: 99%

The role of oxidative stress on the pathophysiology of metabolic syndrome

Francisqueti

Chiaverini

Santos

et al. 2017

Rev. Assoc. Med. Bras.

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“…Pathways involving the activation of melanocortin 4 receptors (MC4) is a key common mechanism mediating the increases in renal sympathetic nerve activity (RSNA) induced by leptin and insulin (Rahmouni et al, 2003), suggesting the potential for an interaction on RSNA, such that increased levels of both hormones could result in an additive action on RSNA. Interestingly both insulin and leptin can regulate each other's production and release, such that an increase in plasma levels of insulin can lead to an increase in leptin levels and vice versa (Santos et al, 2000; Borer, 2014), which further suggests potential interactions of the two hormones. Thus, in order to explore the possibility that insulin and leptin interact within the brain to induce greater increases in RSNA, the first aim of the present study was to compare RSNA in response to administration of leptin and insulin alone and in combination.…”

Section: Introductionmentioning

confidence: 99%

Central Administration of Insulin and Leptin Together Enhance Renal Sympathetic Nerve Activity and Fos Production in the Arcuate Nucleus

et al. 2017

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There is considerable interest in the central actions of insulin and leptin. Both induce sympatho-excitation. This study (i) investigated whether centrally administered leptin and insulin together elicits greater increases in renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate (HR) than when given alone, and (ii) quantified the number of activated neurons in brain regions influencing SNA, to identify potential central sites of interaction. In anesthetised (urethane 1.4–1.6 g/kg iv) male Sprague-Dawley rats, RSNA, MAP, and HR were recorded following intracerebroventricular (ICV) saline (control; n = 5), leptin (7 μg; n = 5), insulin (500 mU; n = 4) and the combination of leptin and insulin; (n = 4). Following leptin or insulin alone, RSNA was significantly increased (74 and 62% respectively). MAP responses were not significantly different between the groups. Insulin alone significantly increased HR. Leptin alone also increased HR but it was significantly less than following insulin alone (P < 0.005). When leptin and insulin were combined, the RSNA increase (124%) was significantly greater than the response to either alone. There were no differences between the groups in MAP responses, however, the increase in HR induced by insulin was attenuated by leptin. Of the brain regions examined, only in the arcuate nucleus did leptin and insulin together increase the number of Fos-positive cell nuclei significantly more than leptin or insulin alone. In the lamina terminalis and rostroventrolateral medulla, leptin and insulin together increased Fos, but the effect was not greater than leptin alone. The results suggest that when central leptin and insulin levels are elevated, the sympatho-excitatory response in RSNA will be greater. The arcuate nucleus may be a common site of cardiovascular integration.

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“…Insulin stimulates leptin release during meal-eating, and leptin then restrains all four of the insulin's actions as well as insulin release. It indirectly counter-regulates the energy storage actions of insulin by promoting lipolysis and stimulation of lipid metabolism (Borer, 2014). This endocrine counter-regulation of short-term energy balance is disrupted in obesity by the resistance of peripheral tissues to the actions of both insulin and leptin.…”

Section: The Endocrine Basis Of Obesity-associated Morbiditiesmentioning

confidence: 99%

How does exercise support dietary approaches to weight loss and better health?

Borer

2019

Ann. Kin.

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The rapid global rise of obesity incurs a heavy personal and healthcare burden due to obesity-associated morbidities and shortening of life. The purpose of this review is to provide evidence-based strategies for prevention, reversal, and mitigation of obesity and its sequelae. To that end, this review highlights the features of human physiology that favor fat accretion and interfere with fat loss. Strategies for prevention of obesity include understanding the basis for the strong motivating properties of palatable food, for human inability to consciously detect calories eaten or calories expended through exercise, for metabolic and hormonal adaptations to negative energy balance that drive weight regain, and for evolutionary natural selection which likely led to high human capacity for fat storage. Reversal of obesity is difficult primarily due to metabolic, hormonal, and behavioral reactions to body fat loss. Reduced resting metabolic rate presents a physiological challenge whether the weight loss is achieved through dietary restriction or energy expenditure of exercise. Increased insulin sensitivity after body fat loss drives resynthesis of storage substrates including triglycerides in the adipose tissue, muscle glycogen, and proteins, thus contributing to weight regain. Reduced basal plasma leptin concentration elicits a strong hunger drive. Mitigation of obesity-associated morbidities involves adding exercise energy expenditure to deliberate control of the quantity of food eaten, reducing postprandial hyperinsulinemia by lowering the carbohydrate load of the diet, and exercising after, rather than before, the meals to facilitate improved glucose tolerance.

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Counterregulation of insulin by leptin as key component of autonomic regulation of body weight

Cited by 32 publications

References 332 publications

The role of oxidative stress on the pathophysiology of metabolic syndrome

The role of oxidative stress on the pathophysiology of metabolic syndrome

Central Administration of Insulin and Leptin Together Enhance Renal Sympathetic Nerve Activity and Fos Production in the Arcuate Nucleus

How does exercise support dietary approaches to weight loss and better health?

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