Relationships between thermic effect of food, insulin resistance and autonomic nervous activity

Watanabe, Tomonori; Nomura, Masahiro; Nakayasu, Kimiko; Kawano, Tomohito; Ito, Susumu; Nakaya, Yutaka

doi:10.2152/jmi.53.153

Cited by 17 publications

(17 citation statements)

References 26 publications

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“…Insulin resistance has been shown to be associated with a blunted TEF (39)(40)(41) and may contribute to the differences we showed. In this study, a lower postprandial glucose response to the test meal was seen after the regular meal pattern than after the irregular meal pattern.…”

Section: Discussionmentioning

confidence: 62%

Irregular meal-pattern effects on energy expenditure, metabolism, and appetite regulation: a randomized controlled trial in healthy normal-weight women

Alhussain

Macdonald

Taylor

2016

The American Journal of Clinical Nutrition

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Background: Obesity is increasing in parallel with greater all-day food availability. The latter may promote meal irregularity, dysregulation of the energy balance, and poor metabolic health. Objective: We investigated the effect of meal irregularity on the thermic effect of food (TEF), lipid concentrations, carbohydrate metabolism, subjective appetite, and gut hormones in healthy women. Design: Eleven normal-weight women (18-40 y of age) were recruited in a randomized crossover trial with two 14-d isoenergetic diet periods (identical foods provided and free living) that were separated by a 14-d habitual diet washout period. In period 1, participants followed a regular meal pattern (6 meals/d) or an irregular meal pattern (3-9 meals/d), and in period 2, the alternative meal pattern was followed. Before and after each period, when participants were fasting and for 3 h after intake of a test drink, measurements were taken of energy expenditure, circulating glucose, lipids (fasting only), insulin, glucagon-like peptide 1 (GLP-1), peptide YY (PYY), and ghrelin. An ad libitum test meal was offered. Subjective appetite ratings were assessed while fasting, after the test drink, after the ad libitum meal, and during the intervention. Continuous interstitial glucose monitoring was undertaken for 3 consecutive days during each intervention, and the ambulatory activity pattern was recorded (ambulatory energy expenditure estimation). Results: Regularity was associated with a greater TEF (P , 0.05) and a lower incremental area under the curve (iAUC) for glucose after intake of the test drink (over 3 h) and, for some identical meals, during the 2 interventions (over 90 min) (day 7: after breakfast; day 9: after lunch and dinner). There was no difference between treatments for the test-drink gut hormone response. A time effect was noted for fasting GLP-1, fasting PYY, PYY responses, and hunger-rating responses to the test drink (P , 0.05). Lower hunger and higher fullness ratings were seen premeal and postmeal during the regular period while subjects were free living. Conclusion: Meal regularity appears to be associated with greater TEF and lower glucose responses, which may favor weight management and metabolic health. This trial was registered at clinicaltrials.gov as NCT02052076.Am J Clin Nutr 2016;104:21-32.

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Section: Discussionmentioning

confidence: 62%

Irregular meal-pattern effects on energy expenditure, metabolism, and appetite regulation: a randomized controlled trial in healthy normal-weight women

Alhussain

Macdonald

Taylor

2016

The American Journal of Clinical Nutrition

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“…In obesity, this means a reduction in the ability of sympathetic hyperactivity to increase metabolic rate and energy consumption, i.e. to have a thermogenic effect that counterbalances the adipose tissue accumulation, ultimately with a further increase in body weight [99]. This receptor abnormality, which is believed to account for the 'fattening effect' associated with prolonged b-blocker treatment [100], may play an even greater role when obesity is associated with hypertension (a common condition in the metabolic syndrome), because under this circumstance sympathetic hyperactivity, and thus presumably adrenoceptor downregulation, is even more pronounced than when obesity or hypertension occur alone [81].…”

Section: Adrenoceptor Downregulationmentioning

confidence: 99%

The sympathetic nervous system and the metabolic syndrome

Mancia

Bousquet

et al. 2007

Journal of Hypertension

346

239

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Studies performed in the past two decades have unequivocally shown that several of the components of the metabolic syndrome are associated with indirect and direct markers of adrenergic overdrive. This is the case for hypertension and obesity, in which resting tachycardia, elevated plasma norepinephrine values, increased sympathetic nerve traffic, as well as augmented levels of total and regional norepinephrine spillover have been reported. This is also the case for insulin resistance, i.e. a metabolic condition frequently complicating the various components of the pathological condition identified as the 'metabolic syndrome'. After briefly describing the epidemiological and the cardiovascular risk profile of the disease, this paper will examine the behaviour of the sympathetic nervous system in the metabolic syndrome as well as the mechanisms potentially responsible for this neurogenic abnormality. This will be followed by an analysis of the role played by neuroadrenergic factors in disease progression as well as in the pathogenesis of its complications. Finally, the therapeutic implications of these findings will be highlighted.

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“…Conversely, some observations suggest a pathogenic role for SNS overactivity in the development and progression of insulin resistance (10,13). SNS activation increases lipolysis, thereby enhancing free fatty acid release and inhibiting glucose transport.…”

Section: Discussionmentioning

confidence: 99%

“…As well, adipose tissue-derived leptin causes sympathetic activation through a hypothalamic pathway that enhances REE (26). Selective leptin resistance in obesity (27), however, counteracts its metabolic effects, whereas the activating effect of leptin on the SNS is preserved (13,28,29). As hyperinsulinaemia, insulin resistance and hyperleptinaemia are hallmarks of obesity, it is difficult to define the initiator of this vicious circle.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, ANS dysfunction is also present in subjects preceding the onset of T2DM, suggesting that the development of ANS impairment parallels the development of obesity, hyperinsulinaemia and insulin resistance (7,8,9) or has a pathogenic role in the development of diabetes (10,11). Once T2DM has developed, chronic hyperglycaemia and persistent increase in sympathetic activity downregulate peripheral b-adrenergic receptors (12,13), resulting in inability of the SNS to enhance energy expenditure (14).…”

Section: Introductionmentioning

confidence: 99%

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Autonomic nervous system activity in diabetic and healthy obese female subjects and the effect of distinct weight loss strategies

Lips

Groot

Kam

et al. 2013

European Journal of Endocrinology

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Objective: Obesity and type 2 diabetes mellitus (T2DM) are reported to be associated with relative overactivity of the sympathetic nervous system (SNS), which is reversible by weight loss. However, direct effects of weight loss by calorie restriction vs Roux-en-Y gastric bypass (RYGB) on SNS overactivity were not studied in parallel. This study compared the effects of RYGB vs restrictive weight loss in obese patients with normal glucose tolerance (NGT) and with T2DM on SNS function as measured by heart rate variability (HRV). Design and methods: Lean (nZ12), obese NGT (nZ27) and T2DM (nZ27) subjects were included in this study. Weight reduction in NGT subjects was achieved by gastric banding (GB) or RYGB and in T2DM subjects by RYGB or high-protein very-low-calorie diet (VLCD). HRV analysis was performed and blood samples were taken at baseline, 3 weeks and 3 months after intervention. Results: At baseline, T2DM subjects showed SNS overactivity and NGT subjects showed similar, but non-significant, findings when compared with lean controls. Weight loss after 3 weeks was comparable in all treatment groups, whereas after 3 months, weight loss was most in VLCD and RYGB subjects. RYGB and VLCD treatment reduced SNS activity within 3 weeks in T2DM patients. After 3 months, restoration to normal autonomic nervous system activity was evident for all groups, except for the NGT-GB group. Conclusion: We can conclude that SNS overactivity is more pronounced in obese T2DM subjects when compared with NGT subjects. Reduction of SNS overactivity coincides with weight loss with the timecourse of reduction dependent on the type of intervention. Surgery or caloric restriction may transiently induce SNS overactivity but do not prevent a direct restoration of sympathovagal balance.

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Relationships between thermic effect of food, insulin resistance and autonomic nervous activity

Abstract: The findings suggest that a reduction in insulin sensitivity induces a poor response of sympathetic nervous activity in the postprandial phase and a reduction in postprandial energy expenditure.

Cited by 17 publications

References 26 publications

Irregular meal-pattern effects on energy expenditure, metabolism, and appetite regulation: a randomized controlled trial in healthy normal-weight women

Irregular meal-pattern effects on energy expenditure, metabolism, and appetite regulation: a randomized controlled trial in healthy normal-weight women

The sympathetic nervous system and the metabolic syndrome

Autonomic nervous system activity in diabetic and healthy obese female subjects and the effect of distinct weight loss strategies

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