Incretin-based approaches for type 2 diabetes therapy: effects on circulating cytokines and adipocyte’s secretome

Jul 17, 2025BMC endocrine disorders

How diabetes treatments that boost gut hormones affect blood immune signals and fat cell secretions

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Abstract

A decline in BMI, HbA1c, and fasting blood glucose occurred 6 months after bariatric surgery (BS) or semaglutide therapy.

Insulin sensitivity significantly increased only after bariatric surgery.
Semaglutide therapy resulted in elevated levels of angiogenic and proinflammatory in the adipocyte secretory profile.
Bariatric surgery also increased proinflammatory cytokines in both adipocyte secretome and plasma levels.
The adipocyte secretome after bariatric surgery showed a reduced proinflammatory response compared to semaglutide therapy.
Semaglutide injections may alter the function of adipose-derived stem cells (ADSC), promoting angiogenesis and adipogenesis.

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BACKGROUND: plays a crucial role in the mechanisms of metabolic diseases. Weight loss has a favourable effect on the adipose tissue secretome and prevents the development of type 2 diabetes mellitus (T2DM) and its complications. The most effective methods of glycaemic control are bariatric surgery (BS) and pharmacotherapy. The aim of our study is to evaluate changes in adipose tissue secretome after BS and semaglutide injections.

METHODS: 17 patients with T2DM were examined before and 6 months after BS or semaglutide therapy. The examination protocol included anthropometry, clinical biochemistry, insulin resistance evaluation and collection of subcutaneous adipose tissue biopsies. Adipose derived stem cells (ADSC) were isolated from biopsies according to a standard enzymatic protocol and differentiated into white and beige adipocytes. Adipogenesis and thermogenesis were assessed by confocal microscopy. Secretome of adipocytes and plasma levels were analyzed using a MILLIPLEX panel.

RESULTS: Following BS and semaglutide therapy, a decline in BMI, total fat content, HbA1c, and fasting blood glucose was observed. Insulin sensitivity increased only 6 months after BS. Semaglutide therapy resulted in the elevation of angiogenic and proinflammatory cytokines in adipocyte secretory profile. After BS we also detected the increase in proinflammatory cytokines both in adipocyte secretome and in plasma levels. However, the adipocyte secretome subsequent to bariatric surgery (BS) exhibited a reduced proinflammatory response in comparison to that observed following semaglutide therapy.

CONCLUSIONS: The effect of semaglutide injections directly on adipose tissue can change the function of ADSC, making them more angiogenic and adipogenic. A decrease in BMI, HbA1c and insulin resistance is achieved to a significant extent only after BS. BS-induced T2DM remission is related to lower pro-inflammatory secretion from adipocytes as compared to semaglutide. The regulation of inflammation in adipocytes may serve as a potential mechanism underlying BS-induced T2DM remission.

Key numbers

51.5 kg/m² to 38.4 kg/m²

BMI Reduction after BS

Median BMI values before and after bariatric surgery

< 6.5%

HbA1c Reduction after BS

Criteria for T2DM remission post-bariatric surgery

70.5 kg to 47.5 kg

Total Fat Content Reduction after BS

Total fat content before and after bariatric surgery

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Incretin-based approaches for type 2 diabetes therapy: effects on circulating cytokines and adipocyte’s secretome

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